Identification of Prominin‐2 as a new player of cardiomyocyte senescence in the aging heart

The aging heart is characterized by a number of structural changes leading to ventricular stiffness, impaired resistance to stress and increased risk of developing heart failure (HF). Genetic or pharmacological removal of senescent cells has recently demonstrated the possibility to relieve some card...

Full description

Saved in:
Bibliographic Details
Published inAging cell Vol. 23; no. 9; pp. e14204 - n/a
Main Authors Maggiorani, D., Santin, Y., Formoso, K., Drapé, E., Martini, H., Brun, S., Cousin, G., Lairez, O., Lezoualc'h, F., Parini, A., Douin‐Echinard, V., Mialet‐Perez, J.
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.09.2024
Wiley Open Access
John Wiley and Sons Inc
Subjects
AC133 Antigen - genetics
AC133 Antigen - metabolism
Aging
Aging - genetics
Aging - metabolism
Aging - physiology
Animals
Biochemistry, Molecular Biology
Cardiology and cardiovascular system
cardiomyocyte
Cardiomyocytes
Cardiomyopathy
Cardiovascular disease
Cell cycle
Cellular Senescence - genetics
Congestive heart failure
Coronary artery disease
Cytokines
Cytotoxicity
DNA damage
Doxorubicin
Ejection fraction
Fibrosis
Genomics
heart
Heart diseases
Heart failure
Heart Failure - genetics
Heart Failure - metabolism
Heart Failure - pathology
Human health and pathology
Humans
Hypertrophy
Ischemia
Kinases
Laboratory animals
Life Sciences
Male
Mice
Mice, Inbred C57BL
Myocytes, Cardiac - metabolism
Oxidative stress
p53 Protein
Senescence
Surgery
Telomeres
Transcriptomics
France
United States > US
senescence
aging
heart
cardiomyocyte
Online AccessGet full text

Cover

Abstract The aging heart is characterized by a number of structural changes leading to ventricular stiffness, impaired resistance to stress and increased risk of developing heart failure (HF). Genetic or pharmacological removal of senescent cells has recently demonstrated the possibility to relieve some cardiac aging features such as hypertrophy and fibrosis. However, the contribution of the different cell types in cardiac aging remains fragmentary due to a lack of cell‐specific markers. Cardiomyocytes undergo post‐mitotic senescence in response to telomere damage, characterized by persistent DNA damage response and expression of the classical senescence markers p21 and p16, which are shared by many other cell types. In the present study, we used transcriptomic approaches to discover new markers specific for cardiomyocyte senescence. We identified Prominin2 (Prom2), encoding a transmembrane glycoprotein, as the most upregulated gene in cardiomyocytes of aged mice compared to young mice. We showed that Prom2 was upregulated by a p53‐dependent pathway in stress‐induced premature senescence. Prom2 expression correlated with cardiomyocyte hypertrophy in the hearts of aged mice and was increased in atrial samples of patients with HF with preserved ejection fraction. Consistently, Prom2 overexpression was sufficient to drive senescence, hypertrophy and resistance to cytotoxic stress while Prom2 shRNA silencing inhibited these features in doxorubicin‐treated cardiac cells. In conclusion, we identified Prom2 as a new player of cardiac aging, linking cardiomyocyte hypertrophy to senescence. These results could provide a better understanding and targeting of cell‐type specific senescence in age‐associated cardiac diseases. Aged cardiomyocytes specifically express a transmembrane glycoprotein Prominin2 (Prom2), with unknown function in the heart. Prom2 expression correlates with cardiomyocyte hypertrophy in hearts of aged mice and is increased in atrial samples of old patients with heart failure with preserved ejection fraction (HFpEF). Prom2 expression can be regulated by a p53‐dependent signaling pathway. In vitro, Prom2 overexpression is sufficient to drive DNA damage, senescence, SASP and resistance to cell death while Prom2 shRNA silencing inhibits these features.
AbstractList The aging heart is characterized by a number of structural changes leading to ventricular stiffness, impaired resistance to stress and increased risk of developing heart failure (HF). Genetic or pharmacological removal of senescent cells has recently demonstrated the possibility to relieve some cardiac aging features such as hypertrophy and fibrosis. However, the contribution of the different cell types in cardiac aging remains fragmentary due to a lack of cell-specific markers. Cardiomyocytes undergo post-mitotic senescence in response to telomere damage, characterized by persistent DNA damage response and expression of the classical senescence markers p21 and p16, which are shared by many other cell types. In the present study, we used transcriptomic approaches to discover new markers specific for cardiomyocyte senescence. We identified Prominin2 (Prom2), encoding a transmembrane glycoprotein, as the most upregulated gene in cardiomyocytes of aged mice compared to young mice. We showed that Prom2 was upregulated by a p53-dependent pathway in stress-induced premature senescence. Prom2 expression correlated with cardiomyocyte hypertrophy in the hearts of aged mice and was increased in atrial samples of patients with HF with preserved ejection fraction. Consistently, Prom2 overexpression was sufficient to drive senescence, hypertrophy and resistance to cytotoxic stress while Prom2 shRNA silencing inhibited these features in doxorubicin-treated cardiac cells. In conclusion, we identified Prom2 as a new player of cardiac aging, linking cardiomyocyte hypertrophy to senescence. These results could provide a better understanding and targeting of cell-type specific senescence in age-associated cardiac diseases.The aging heart is characterized by a number of structural changes leading to ventricular stiffness, impaired resistance to stress and increased risk of developing heart failure (HF). Genetic or pharmacological removal of senescent cells has recently demonstrated the possibility to relieve some cardiac aging features such as hypertrophy and fibrosis. However, the contribution of the different cell types in cardiac aging remains fragmentary due to a lack of cell-specific markers. Cardiomyocytes undergo post-mitotic senescence in response to telomere damage, characterized by persistent DNA damage response and expression of the classical senescence markers p21 and p16, which are shared by many other cell types. In the present study, we used transcriptomic approaches to discover new markers specific for cardiomyocyte senescence. We identified Prominin2 (Prom2), encoding a transmembrane glycoprotein, as the most upregulated gene in cardiomyocytes of aged mice compared to young mice. We showed that Prom2 was upregulated by a p53-dependent pathway in stress-induced premature senescence. Prom2 expression correlated with cardiomyocyte hypertrophy in the hearts of aged mice and was increased in atrial samples of patients with HF with preserved ejection fraction. Consistently, Prom2 overexpression was sufficient to drive senescence, hypertrophy and resistance to cytotoxic stress while Prom2 shRNA silencing inhibited these features in doxorubicin-treated cardiac cells. In conclusion, we identified Prom2 as a new player of cardiac aging, linking cardiomyocyte hypertrophy to senescence. These results could provide a better understanding and targeting of cell-type specific senescence in age-associated cardiac diseases.
The aging heart is characterized by a number of structural changes leading to ventricular stiffness, impaired resistance to stress and increased risk of developing heart failure (HF). Genetic or pharmacological removal of senescent cells has recently demonstrated the possibility to relieve some cardiac aging features such as hypertrophy and fibrosis. However, the contribution of the different cell types in cardiac aging remains fragmentary due to a lack of cell‐specific markers. Cardiomyocytes undergo post‐mitotic senescence in response to telomere damage, characterized by persistent DNA damage response and expression of the classical senescence markers p21 and p16, which are shared by many other cell types. In the present study, we used transcriptomic approaches to discover new markers specific for cardiomyocyte senescence. We identified Prominin2 (Prom2), encoding a transmembrane glycoprotein, as the most upregulated gene in cardiomyocytes of aged mice compared to young mice. We showed that Prom2 was upregulated by a p53‐dependent pathway in stress‐induced premature senescence. Prom2 expression correlated with cardiomyocyte hypertrophy in the hearts of aged mice and was increased in atrial samples of patients with HF with preserved ejection fraction. Consistently, Prom2 overexpression was sufficient to drive senescence, hypertrophy and resistance to cytotoxic stress while Prom2 shRNA silencing inhibited these features in doxorubicin‐treated cardiac cells. In conclusion, we identified Prom2 as a new player of cardiac aging, linking cardiomyocyte hypertrophy to senescence. These results could provide a better understanding and targeting of cell‐type specific senescence in age‐associated cardiac diseases.
The aging heart is characterized by a number of structural changes leading to ventricular stiffness, impaired resistance to stress and increased risk of developing heart failure (HF). Genetic or pharmacological removal of senescent cells has recently demonstrated the possibility to relieve some cardiac aging features such as hypertrophy and fibrosis. However, the contribution of the different cell types in cardiac aging remains fragmentary due to a lack of cell‐specific markers. Cardiomyocytes undergo post‐mitotic senescence in response to telomere damage, characterized by persistent DNA damage response and expression of the classical senescence markers p21 and p16, which are shared by many other cell types. In the present study, we used transcriptomic approaches to discover new markers specific for cardiomyocyte senescence. We identified Prominin2 (Prom2), encoding a transmembrane glycoprotein, as the most upregulated gene in cardiomyocytes of aged mice compared to young mice. We showed that Prom2 was upregulated by a p53‐dependent pathway in stress‐induced premature senescence. Prom2 expression correlated with cardiomyocyte hypertrophy in the hearts of aged mice and was increased in atrial samples of patients with HF with preserved ejection fraction. Consistently, Prom2 overexpression was sufficient to drive senescence, hypertrophy and resistance to cytotoxic stress while Prom2 shRNA silencing inhibited these features in doxorubicin‐treated cardiac cells. In conclusion, we identified Prom2 as a new player of cardiac aging, linking cardiomyocyte hypertrophy to senescence. These results could provide a better understanding and targeting of cell‐type specific senescence in age‐associated cardiac diseases. Aged cardiomyocytes specifically express a transmembrane glycoprotein Prominin2 (Prom2), with unknown function in the heart. Prom2 expression correlates with cardiomyocyte hypertrophy in hearts of aged mice and is increased in atrial samples of old patients with heart failure with preserved ejection fraction (HFpEF). Prom2 expression can be regulated by a p53‐dependent signaling pathway. In vitro, Prom2 overexpression is sufficient to drive DNA damage, senescence, SASP and resistance to cell death while Prom2 shRNA silencing inhibits these features.
Author Cousin, G.
Formoso, K.
Parini, A.
Douin‐Echinard, V.
Santin, Y.
Lezoualc'h, F.
Lairez, O.
Maggiorani, D.
Brun, S.
Mialet‐Perez, J.
Martini, H.
Drapé, E.
AuthorAffiliation 1 Institute of Metabolic and Cardiovascular Diseases (I2MC), UMR‐1297 INSERM, University of Toulouse Toulouse France
2 Rangueil Hospital, CHU Toulouse France
4 Univ Angers, INSERM, CNRS, MITOVASC, Equipe MitoLab, SFR ICAT Angers France
3 RESTORE Research Center, UMR‐1301, INSERM, CNRS, EFS University of Toulouse Toulouse France
AuthorAffiliation_xml – name: 4 Univ Angers, INSERM, CNRS, MITOVASC, Equipe MitoLab, SFR ICAT Angers France
– name: 1 Institute of Metabolic and Cardiovascular Diseases (I2MC), UMR‐1297 INSERM, University of Toulouse Toulouse France
– name: 3 RESTORE Research Center, UMR‐1301, INSERM, CNRS, EFS University of Toulouse Toulouse France
– name: 2 Rangueil Hospital, CHU Toulouse France
Author_xml – sequence: 1
  givenname: D.
  surname: Maggiorani
  fullname: Maggiorani, D.
  organization: Institute of Metabolic and Cardiovascular Diseases (I2MC), UMR‐1297 INSERM, University of Toulouse
– sequence: 2
  givenname: Y.
  surname: Santin
  fullname: Santin, Y.
  organization: Institute of Metabolic and Cardiovascular Diseases (I2MC), UMR‐1297 INSERM, University of Toulouse
– sequence: 3
  givenname: K.
  surname: Formoso
  fullname: Formoso, K.
  organization: Institute of Metabolic and Cardiovascular Diseases (I2MC), UMR‐1297 INSERM, University of Toulouse
– sequence: 4
  givenname: E.
  surname: Drapé
  fullname: Drapé, E.
  organization: Institute of Metabolic and Cardiovascular Diseases (I2MC), UMR‐1297 INSERM, University of Toulouse
– sequence: 5
  givenname: H.
  surname: Martini
  fullname: Martini, H.
  organization: Rangueil Hospital, CHU
– sequence: 6
  givenname: S.
  surname: Brun
  fullname: Brun, S.
  organization: Rangueil Hospital, CHU
– sequence: 7
  givenname: G.
  surname: Cousin
  fullname: Cousin, G.
  organization: Rangueil Hospital, CHU
– sequence: 8
  givenname: O.
  surname: Lairez
  fullname: Lairez, O.
  organization: Rangueil Hospital, CHU
– sequence: 9
  givenname: F.
  surname: Lezoualc'h
  fullname: Lezoualc'h, F.
  organization: Institute of Metabolic and Cardiovascular Diseases (I2MC), UMR‐1297 INSERM, University of Toulouse
– sequence: 10
  givenname: A.
  orcidid: 0000-0002-9848-8838
  surname: Parini
  fullname: Parini, A.
  organization: Institute of Metabolic and Cardiovascular Diseases (I2MC), UMR‐1297 INSERM, University of Toulouse
– sequence: 11
  givenname: V.
  surname: Douin‐Echinard
  fullname: Douin‐Echinard, V.
  email: victorine.douin@inserm.fr
  organization: University of Toulouse
– sequence: 12
  givenname: J.
  surname: Mialet‐Perez
  fullname: Mialet‐Perez, J.
  email: jeanne.perez@inserm.fr
  organization: Univ Angers, INSERM, CNRS, MITOVASC, Equipe MitoLab, SFR ICAT
BackLink https://www.ncbi.nlm.nih.gov/pubmed/38757782$$D View this record in MEDLINE/PubMed
https://hal.science/hal-04618754$$DView record in HAL
BookMark eNp9ks1O3DAQxy0EKh_thQeoLHEpSEvt2Os4p2q1ooC0Ej20x8pynMmuUWJv7Swotz5Cn5EnqUNgBRywDx55fjPz18wcol3nHSB0TMk5TeerNtCcU54RvoMOKM_5pMgzsbu1qdxHhzHeEkLzgrAPaJ_JfJrnMjtAv68rcJ2trdGd9Q77Gv8IvrXOuoe__zKsI9bYwT1eN7qHMPiNDpX1be9N3wGO4CAacAawdbhbAdZL65Z4BTp0H9FerZsIn57eI_Tr-8XP-dVkcXN5PZ8tJobzjE8qIYlIWg0pichISWlJcimKOpmCsILUpS6gFLVg1IiKVwUnekp1ugkqCTtC38a8603ZQpXkdEE3ah1sq0OvvLbqtcfZlVr6O0Upl5JxljKcjhlWb-KuZgs1_BEuaOoav6OJ_fJULfg_G4idam1qQdNoB34TFSNTIQST2YCevEFv_Sa41AvFaJoGy5gc5H9-KX9b_3lMCTgbARN8jAHqLUKJGnZADTugHncgwXSE720D_Tukms0vFmPMfzrKskw
Cites_doi 10.1016/j.jacc.2010.12.032
10.1038/s41591‐018‐0059‐x
10.1038/s41467‐022‐34801‐9
10.1111/febs.16351
10.1161/CIRCRESAHA.111.247866
10.1016/S0022-2828(03)00084-1
10.1038/s41417‐019‐0109‐7
10.1161/CIRCULATIONAHA.117.031358
10.3390/ijms22052245
10.1038/nature20099
10.15252/embj.2018100492
10.1016/j.devcel.2019.10.007
10.1111/acel.12811
10.1038/nature16932
10.1172/JCI162519
10.1016/j.bbrc.2013.03.097
10.1016/j.phrs.2022.106356
10.1097/FJC.0000000000000878
10.1111/acel.13753
10.1042/EBC20170022
10.1038/s41569‐021‐00624‐2
10.1016/j.mad.2021.111540
10.1016/j.jaccao.2023.03.012
10.1074/jbc.M210640200
10.1016/s0008‐6363(02)00660‐0
10.1111/acel.12931
10.3389/fgene.2013.00024
10.1111/acel.13015
10.1016/j.jacbts.2017.12.006
10.1126/scisignal.abn8017
10.1016/j.cell.2017.02.004
10.1016/j.mad.2022.111740
10.1007/s00441‐006‐0324‐z
10.1038/nrc3960
10.1128/MCB.21.10.3375‐3386.2001
10.1093/eurjhf/hft028
10.1161/CIRCULATIONAHA.121.054204
10.1089/ars.2012.4616
10.15252/emmm.202013792
10.1038/s41586‐020‐2496‐1
10.4161/auto.6.5.11947
10.1158/2159‐8290.CD‐16‐0241
10.1016/j.bbrc.2007.01.089
10.1111/acel.12945
10.1080/10985549.2023.2229225
10.1177/1933719117737842
10.1172/JCI22475
10.15420/cfr.2022.06
10.1111/acel.13249
10.1161/CIRCRESAHA.109.198366
10.1016/j.ceb.2017.02.014
10.1016/j.yjmcc.2011.07.019
10.1111/acel.12344
10.1038/nature09787
10.1161/CIRCULATIONAHA.109.871137
10.1038/s41569‐023‐00881‐3
ContentType Journal Article
Copyright 2024 The Authors. published by Anatomical Society and John Wiley & Sons Ltd.
2024 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd.
2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Attribution
Copyright_xml – notice: 2024 The Authors. published by Anatomical Society and John Wiley & Sons Ltd.
– notice: 2024 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd.
– notice: 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
– notice: Attribution
DBID 24P
AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7QP
7TK
8FE
8FH
ABUWG
AFKRA
AZQEC
BBNVY
BENPR
BHPHI
CCPQU
DWQXO
GNUQQ
HCIFZ
LK8
M7P
PHGZM
PHGZT
PIMPY
PKEHL
PQEST
PQGLB
PQQKQ
PQUKI
PRINS
7X8
1XC
VOOES
5PM
DOI 10.1111/acel.14204
DatabaseName Wiley Online Library Open Access
CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
Calcium & Calcified Tissue Abstracts
Neurosciences Abstracts
ProQuest SciTech Collection
ProQuest Natural Science Collection
ProQuest Central (Alumni)
ProQuest Central UK/Ireland
ProQuest Central Essentials
Biological Science Collection
ProQuest Central
Natural Science Collection
ProQuest One Community College
ProQuest Central
ProQuest Central Student
SciTech Premium Collection
Biological Sciences
Biological Science Database
ProQuest Central Premium
ProQuest One Academic (New)
Publicly Available Content Database
ProQuest One Academic Middle East (New)
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Applied & Life Sciences
ProQuest One Academic
ProQuest One Academic UKI Edition
ProQuest Central China
MEDLINE - Academic
Hyper Article en Ligne (HAL)
Hyper Article en Ligne (HAL) (Open Access)
PubMed Central (Full Participant titles)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
Publicly Available Content Database
ProQuest Central Student
ProQuest One Academic Middle East (New)
ProQuest Biological Science Collection
ProQuest Central Essentials
ProQuest One Academic Eastern Edition
ProQuest Central (Alumni Edition)
SciTech Premium Collection
ProQuest One Community College
ProQuest Natural Science Collection
Biological Science Database
ProQuest SciTech Collection
Neurosciences Abstracts
ProQuest Central China
ProQuest Central
ProQuest One Applied & Life Sciences
ProQuest One Academic UKI Edition
Natural Science Collection
ProQuest Central Korea
Biological Science Collection
ProQuest Central (New)
ProQuest One Academic
Calcium & Calcified Tissue Abstracts
ProQuest One Academic (New)
MEDLINE - Academic
DatabaseTitleList MEDLINE - Academic

CrossRef
MEDLINE


Publicly Available Content Database
Database_xml – sequence: 1
  dbid: 24P
  name: Wiley Online Library Open Access
  url: https://authorservices.wiley.com/open-science/open-access/browse-journals.html
  sourceTypes: Publisher
– sequence: 2
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 3
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
– sequence: 4
  dbid: BENPR
  name: ProQuest Central
  url: https://www.proquest.com/central
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Biology
DocumentTitleAlternate Maggiorani et al
EISSN 1474-9726
1474-9728
EndPage n/a
ExternalDocumentID PMC11488343
oai_HAL_hal_04618754v1
38757782
10_1111_acel_14204
ACEL14204
Genre researchArticle
Journal Article
GeographicLocations France
United States--US
GeographicLocations_xml – name: France
– name: United States--US
GrantInformation_xml – fundername: Fondation pour la Recherche Médicale
  funderid: EQU202103012601
– fundername: Région Occitanie Pyrénées‐Méditerranée
– fundername: Agence Nationale de la Recherche
  funderid: ANR‐19‐CE14‐0038‐01
– fundername: Fédération Francaise de Cardiologie
– fundername: Conseil Régional des Pays de la Loire
– fundername: Fondation Lefoulon‐Delalande
– fundername: Fondation Lefoulon-Delalande
– fundername: Région Occitanie Pyrénées-Méditerranée
– fundername: Agence Nationale de la Recherche
  grantid: ANR-19-CE14-0038-01
– fundername: Fondation pour la Recherche Médicale
  grantid: EQU202103012601
GroupedDBID ---
.3N
.GA
.Y3
05W
0R~
10A
1OC
23M
24P
2WC
31~
36B
4.4
50Y
50Z
51W
51X
52M
52N
52O
52P
52R
52S
52T
52W
52X
53G
5GY
5HH
5LA
5VS
66C
6J9
702
7PT
8-0
8-1
8-3
8-4
8-5
8FE
8FH
8UM
930
A01
A03
AAHHS
AAZKR
ABCQN
ABDBF
ABEML
ABJNI
ACCFJ
ACCMX
ACGFO
ACGFS
ACPRK
ACSCC
ACUHS
ACXQS
ADBBV
ADKYN
ADRAZ
ADZMN
ADZOD
AEEZP
AEGXH
AENEX
AEQDE
AFBPY
AFEBI
AFKRA
AFZJQ
AIAGR
AIWBW
AJBDE
ALMA_UNASSIGNED_HOLDINGS
ALUQN
AOIJS
AVUZU
BAWUL
BBNVY
BCNDV
BENPR
BFHJK
BHPHI
BY8
CAG
CCPQU
COF
CS3
D-6
D-7
D-E
D-F
DIK
DR2
E3Z
EAD
EAP
EBD
EBS
EJD
EMB
EMK
EMOBN
EST
ESX
F00
F01
F04
F5P
FIJ
GODZA
GROUPED_DOAJ
GX1
HCIFZ
HF~
HOLLA
HZ~
IAO
IHE
IHR
IPNFZ
ITC
IX1
J0M
K.9
KQ8
LC2
LC3
LH4
LK8
LP6
LP7
LW6
M48
M7P
MK4
N04
N05
N9A
O9-
OBS
OIG
OK1
OVD
P2P
P2X
P2Z
P4B
P4D
PIMPY
Q11
ROL
RPM
RX1
SUPJJ
SV3
TEORI
TR2
TUS
UB1
V8K
W8V
WIN
WQJ
WRC
WXI
XG1
YFH
YUY
~IA
~WT
AAYXX
CITATION
PHGZM
PHGZT
CGR
CUY
CVF
ECM
EIF
NPM
7QP
7TK
AAMMB
ABUWG
AEFGJ
AGXDD
AIDQK
AIDYY
AZQEC
DWQXO
GNUQQ
PKEHL
PQEST
PQGLB
PQQKQ
PQUKI
PRINS
7X8
1XC
VOOES
5PM
ID FETCH-LOGICAL-c4424-d6806474c0b0620b11b07869f0b160390fba9eb6f631c6d4d940a51a1a169fb03
IEDL.DBID M48
ISSN 1474-9718
1474-9726
IngestDate Thu Aug 21 18:31:12 EDT 2025
Fri May 09 12:19:23 EDT 2025
Tue Aug 05 10:07:16 EDT 2025
Wed Aug 13 07:33:38 EDT 2025
Wed Feb 19 02:06:46 EST 2025
Tue Jul 01 01:49:21 EDT 2025
Wed Jan 22 17:13:26 EST 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 9
Keywords senescence
aging
heart
cardiomyocyte
Language English
License Attribution
2024 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd.
Attribution: http://creativecommons.org/licenses/by
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c4424-d6806474c0b0620b11b07869f0b160390fba9eb6f631c6d4d940a51a1a169fb03
Notes D. Maggiorani, Y. Santin and K. Formoso have contributed equally to this work.
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ORCID 0000-0002-9848-8838
0000-0002-1765-0283
0000-0002-0630-7666
0000-0002-9229-1161
0000-0003-4890-8547
OpenAccessLink http://journals.scholarsportal.info/openUrl.xqy?doi=10.1111/acel.14204
PMID 38757782
PQID 3117932380
PQPubID 1036381
PageCount 18
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_11488343
hal_primary_oai_HAL_hal_04618754v1
proquest_miscellaneous_3056663821
proquest_journals_3117932380
pubmed_primary_38757782
crossref_primary_10_1111_acel_14204
wiley_primary_10_1111_acel_14204_ACEL14204
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate September 2024
PublicationDateYYYYMMDD 2024-09-01
PublicationDate_xml – month: 09
  year: 2024
  text: September 2024
PublicationDecade 2020
PublicationPlace England
PublicationPlace_xml – name: England
– name: London
– name: Hoboken
PublicationTitle Aging cell
PublicationTitleAlternate Aging Cell
PublicationYear 2024
Publisher John Wiley & Sons, Inc
Wiley Open Access
John Wiley and Sons Inc
Publisher_xml – name: John Wiley & Sons, Inc
– name: Wiley Open Access
– name: John Wiley and Sons Inc
References 2017; 7
2013; 4
2019; 51
2021; 22
2017; 47
2023; 5
2010; 106
2003; 57
2019; 18
2011; 57
2011; 470
2003; 278
2020; 19
2012; 52
2014; 20
2023; 20
2013; 15
2018; 3
2023; 290
2023; 22
2018; 138
2013; 434
2023; 133
2009; 120
2021; 198
2022; 208
2017; 168
2010; 6
2017; 61
2015; 15
2015; 14
2007; 328
2020; 583
2003; 35
2019; 38
2021; 144
2020; 76
2018; 25
2018; 24
2001; 21
2023; 43
2021; 13
2007; 354
2018; 17
2012; 111
2004; 114
2022; 183
2016; 539
2022; 8
2016; 530
2020; 27
2022; 13
2022; 15
2022; 19
e_1_2_11_32_1
e_1_2_11_55_1
e_1_2_11_30_1
e_1_2_11_57_1
e_1_2_11_36_1
e_1_2_11_51_1
e_1_2_11_13_1
e_1_2_11_34_1
e_1_2_11_53_1
e_1_2_11_11_1
e_1_2_11_29_1
e_1_2_11_6_1
e_1_2_11_27_1
e_1_2_11_4_1
e_1_2_11_48_1
e_1_2_11_2_1
e_1_2_11_20_1
e_1_2_11_45_1
e_1_2_11_47_1
e_1_2_11_24_1
e_1_2_11_41_1
e_1_2_11_8_1
e_1_2_11_22_1
e_1_2_11_43_1
e_1_2_11_17_1
e_1_2_11_15_1
e_1_2_11_38_1
e_1_2_11_19_1
e_1_2_11_50_1
e_1_2_11_10_1
e_1_2_11_31_1
e_1_2_11_56_1
e_1_2_11_14_1
e_1_2_11_35_1
e_1_2_11_52_1
e_1_2_11_12_1
e_1_2_11_33_1
e_1_2_11_54_1
e_1_2_11_7_1
e_1_2_11_28_1
e_1_2_11_5_1
e_1_2_11_26_1
e_1_2_11_3_1
e_1_2_11_49_1
e_1_2_11_21_1
e_1_2_11_44_1
e_1_2_11_46_1
e_1_2_11_25_1
e_1_2_11_40_1
e_1_2_11_9_1
e_1_2_11_23_1
e_1_2_11_42_1
e_1_2_11_18_1
e_1_2_11_16_1
e_1_2_11_37_1
e_1_2_11_39_1
References_xml – volume: 47
  start-page: 117
  year: 2017
  end-page: 125
  article-title: The caveolae dress code: structure and signaling
  publication-title: Current Opinion in Cell Biology
– volume: 138
  start-page: 809
  issue: 8
  year: 2018
  end-page: 822
  article-title: Visceral adipose tissue drives cardiac aging through modulation of fibroblast senescence by osteopontin production
  publication-title: Circulation
– volume: 43
  start-page: 426
  issue: 8
  year: 2023
  end-page: 449
  article-title: Shared gene targets of the ATF4 and p53 transcriptional networks
  publication-title: Molecular and Cellular Biology
– volume: 530
  start-page: 184
  issue: 7589
  year: 2016
  end-page: 189
  article-title: Naturally occurring p16(Ink4a)‐positive cells shorten healthy lifespan
  publication-title: Nature
– volume: 6
  start-page: 600
  issue: 5
  year: 2010
  end-page: 606
  article-title: Inhibition of autophagy in the heart induces age‐related cardiomyopathy
  publication-title: Autophagy
– volume: 22
  issue: 1
  year: 2023
  article-title: Role of autophagy in aging: The good, the bad, and the ugly
  publication-title: Aging Cell
– volume: 61
  start-page: 721
  issue: 6
  year: 2017
  end-page: 732
  article-title: Autophagy in health and disease: Focus on the cardiovascular system
  publication-title: Essays in Biochemistry
– volume: 114
  start-page: 1299
  issue: 9
  year: 2004
  end-page: 1307
  article-title: Ink4a/Arf expression is a biomarker of aging
  publication-title: The Journal of Clinical Investigation
– volume: 15
  start-page: 717
  issue: 7
  year: 2013
  end-page: 723
  article-title: Heart failure in elderly patients: Distinctive features and unresolved issues
  publication-title: European Journal of Heart Failure
– volume: 18
  issue: 3
  year: 2019
  article-title: Pharmacological clearance of senescent cells improves survival and recovery in aged mice following acute myocardial infarction
  publication-title: Aging Cell
– volume: 3
  start-page: 230
  issue: 2
  year: 2018
  end-page: 244
  article-title: CCR2 monocyte‐derived infiltrating macrophages are required for adverse cardiac remodeling during pressure overload
  publication-title: ACC. Basic to Translational Science
– volume: 19
  start-page: 250
  issue: 4
  year: 2022
  end-page: 264
  article-title: The role of cellular senescence in cardiac disease: Basic biology and clinical relevance
  publication-title: Nature Reviews. Cardiology
– volume: 539
  start-page: 54
  issue: 7627
  year: 2016
  end-page: 58
  article-title: Break‐induced telomere synthesis underlies alternative telomere maintenance
  publication-title: Nature
– volume: 354
  start-page: 913
  issue: 4
  year: 2007
  end-page: 918
  article-title: A p53‐type response element in the GDF15 promoter confers high specificity for p53 activation
  publication-title: Biochemical and Biophysical Research Communications
– volume: 583
  start-page: 590
  issue: 7817
  year: 2020
  end-page: 595
  article-title: A single‐cell transcriptomic atlas characterizes ageing tissues in the mouse
  publication-title: Nature
– volume: 434
  start-page: 466
  issue: 3
  year: 2013
  end-page: 472
  article-title: Prominin‐2 expression increases protrusions, decreases caveolae and inhibits Cdc42 dependent fluid phase endocytosis
  publication-title: Biochemical and Biophysical Research Communications
– volume: 290
  start-page: 1235
  issue: 5
  year: 2023
  end-page: 1255
  article-title: Therapeutic opportunities for senolysis in cardiovascular disease
  publication-title: The FEBS Journal
– volume: 8
  year: 2022
  article-title: Epidemiology and clinical features of heart failure with preserved ejection fraction
  publication-title: Cardiac Failure Review
– volume: 38
  issue: 5
  year: 2019
  article-title: Length‐independent telomere damage drives post‐mitotic cardiomyocyte senescence
  publication-title: The EMBO Journal
– volume: 76
  start-page: 452
  issue: 4
  year: 2020
  end-page: 460
  article-title: Senolytic agent navitoclax inhibits angiotensin II‐induced heart failure in mice
  publication-title: Journal of Cardiovascular Pharmacology
– volume: 15
  issue: 758
  year: 2022
  article-title: Doxorubicin causes ferroptosis and cardiotoxicity by intercalating into mitochondrial DNA and disrupting Alas1‐dependent heme synthesis
  publication-title: Science Signaling
– volume: 278
  start-page: 8586
  issue: 10
  year: 2003
  end-page: 8596
  article-title: Characterization of prominin‐2, a new member of the prominin family of pentaspan membrane glycoproteins
  publication-title: The Journal of Biological Chemistry
– volume: 4
  year: 2013
  article-title: Pharmacogenetics of cytochrome P450 2B6 (CYP2B6): Advances on polymorphisms, mechanisms, and clinical relevance
  publication-title: Frontiers in Genetics
– volume: 25
  start-page: 1231
  issue: 8
  year: 2018
  end-page: 1242
  article-title: Prominin‐2 prevents the formation of caveolae in normal and ovarian hyperstimulated pregnancy
  publication-title: Reproductive Sciences
– volume: 13
  issue: 8
  year: 2021
  article-title: Targeting prominin2 transcription to overcome ferroptosis resistance in cancer
  publication-title: EMBO Molecular Medicine
– volume: 35
  start-page: 615
  issue: 6
  year: 2003
  end-page: 621
  article-title: H(2)O(2) regulates cardiac myocyte phenotype via concentration‐dependent activation of distinct kinase pathways
  publication-title: Journal of Molecular and Cellular Cardiology
– volume: 20
  start-page: 754
  issue: 11
  year: 2023
  end-page: 777
  article-title: Hallmarks of cardiovascular ageing
  publication-title: Nature Reviews. Cardiology
– volume: 22
  issue: 5
  year: 2021
  article-title: Selective cardiomyocyte oxidative stress leads to bystander senescence of cardiac stromal cells
  publication-title: International Journal of Molecular Sciences
– volume: 52
  start-page: 502
  issue: 2
  year: 2012
  end-page: 510
  article-title: Serotonin 5‐HT2A receptor‐mediated hypertrophy is negatively regulated by caveolin‐3 in cardiomyoblasts and neonatal cardiomyocytes
  publication-title: Journal of Molecular and Cellular Cardiology
– volume: 19
  year: 2020
  article-title: Clearance of senescent cells during cardiac ischemia‐reperfusion injury improves recovery
  publication-title: Aging Cell
– volume: 183
  year: 2022
  article-title: Pharmacological senolysis reduces doxorubicin‐induced cardiotoxicity and improves cardiac function in mice
  publication-title: Pharmacological Research
– volume: 168
  start-page: 960
  issue: 6
  year: 2017
  end-page: 976
  article-title: mTOR signaling in growth, metabolism, and disease
  publication-title: Cell
– volume: 21
  start-page: 3375
  issue: 10
  year: 2001
  end-page: 3386
  article-title: Kinetics of p53 binding to promoter sites in vivo
  publication-title: Molecular and Cellular Biology
– volume: 51
  start-page: 575
  issue: 5
  year: 2019
  end-page: 586 e574
  article-title: Prominin2 drives ferroptosis resistance by stimulating iron export
  publication-title: Developmental Cell
– volume: 7
  start-page: 165
  issue: 2
  year: 2017
  end-page: 176
  article-title: Cellular senescence promotes adverse effects of chemotherapy and cancer relapse
  publication-title: Cancer Discovery
– volume: 57
  start-page: 2273
  issue: 22
  year: 2011
  end-page: 2283
  article-title: Cardiac‐specific overexpression of caveolin‐3 attenuates cardiac hypertrophy and increases natriuretic peptide expression and signaling
  publication-title: Journal of the American College of Cardiology
– volume: 328
  start-page: 31
  issue: 1
  year: 2007
  end-page: 47
  article-title: Prominin‐2 is a cholesterol‐binding protein associated with apical and basolateral plasmalemmal protrusions in polarized epithelial cells and released into urine
  publication-title: Cell and Tissue Research
– volume: 17
  issue: 5
  year: 2018
  article-title: Monoamine oxidase‐a is a novel driver of stress‐induced premature senescence through inhibition of parkin‐mediated mitophagy
  publication-title: Aging Cell
– volume: 120
  start-page: 1695
  issue: 17
  year: 2009
  end-page: 1703
  article-title: Suppression of phosphoinositide 3‐kinase prevents cardiac aging in mice
  publication-title: Circulation
– volume: 198
  year: 2021
  article-title: Senescence and senolytics in cardiovascular disease: Promise and potential pitfalls
  publication-title: Mechanisms of Ageing and Development
– volume: 13
  start-page: 7028
  issue: 1
  year: 2022
  article-title: A Glb1‐2A‐mCherry reporter monitors systemic aging and predicts lifespan in middle‐aged mice
  publication-title: Nature Communications
– volume: 111
  start-page: 97
  issue: 1
  year: 2012
  end-page: 109
  article-title: Assessing cell and organ senescence biomarkers
  publication-title: Circulation Research
– volume: 144
  start-page: 559
  issue: 7
  year: 2021
  end-page: 574
  article-title: Dysregulated phenylalanine catabolism plays a key role in the trajectory of cardiac aging
  publication-title: Circulation
– volume: 14
  start-page: 644
  issue: 4
  year: 2015
  end-page: 658
  article-title: The Achilles' heel of senescent cells: From transcriptome to senolytic drugs
  publication-title: Aging Cell
– volume: 5
  start-page: 298
  issue: 3
  year: 2023
  end-page: 315
  article-title: Evaluation of senescence and its prevention in doxorubicin‐induced cardiotoxicity using dynamic engineered heart tissues
  publication-title: JACC. CardioOncology
– volume: 18
  issue: 3
  year: 2019
  article-title: Aged‐senescent cells contribute to impaired heart regeneration
  publication-title: Aging Cell
– volume: 208
  year: 2022
  article-title: Pharmacological clearance of senescent cells improves cardiac remodeling and function after myocardial infarction in female aged mice
  publication-title: Mechanisms of Ageing and Development
– volume: 20
  start-page: 267
  issue: 2
  year: 2014
  end-page: 280
  article-title: Monoamine oxidase B prompts mitochondrial and cardiac dysfunction in pressure overloaded hearts
  publication-title: Antioxidants & Redox Signaling
– volume: 57
  start-page: 358
  issue: 2
  year: 2003
  end-page: 369
  article-title: Caveolin‐1 and ‐3 dissociations from caveolae to cytosol in the heart during aging and after myocardial infarction in rat
  publication-title: Cardiovascular Research
– volume: 133
  year: 2023
  article-title: Local senolysis in aged mice only partially replicates the benefits of systemic senolysis
  publication-title: The Journal of Clinical Investigation
– volume: 470
  start-page: 359
  issue: 7334
  year: 2011
  end-page: 365
  article-title: Telomere dysfunction induces metabolic and mitochondrial compromise
  publication-title: Nature
– volume: 106
  start-page: 193
  issue: 1
  year: 2010
  end-page: 202
  article-title: Monoamine oxidase A‐mediated enhanced catabolism of norepinephrine contributes to adverse remodeling and pump failure in hearts with pressure overload
  publication-title: Circulation Research
– volume: 15
  start-page: 397
  issue: 7
  year: 2015
  end-page: 408
  article-title: Forging a signature of in vivo senescence
  publication-title: Nature Reviews. Cancer
– volume: 27
  start-page: 147
  issue: 3–4
  year: 2020
  end-page: 167
  article-title: PROM1 and PROM2 expression differentially modulates clinical prognosis of cancer: A multiomics analysis
  publication-title: Cancer Gene Therapy
– volume: 24
  start-page: 1234
  issue: 8
  year: 2018
  end-page: 1245
  article-title: The human heart contains distinct macrophage subsets with divergent origins and functions
  publication-title: Nature Medicine
– volume: 18
  issue: 5
  year: 2019
  article-title: Aging induces cardiac mesenchymal stromal cell senescence and promotes endothelial cell fate of the CD90 + subset
  publication-title: Aging Cell
– ident: e_1_2_11_19_1
  doi: 10.1016/j.jacc.2010.12.032
– ident: e_1_2_11_5_1
  doi: 10.1038/s41591‐018‐0059‐x
– ident: e_1_2_11_48_1
  doi: 10.1038/s41467‐022‐34801‐9
– ident: e_1_2_11_49_1
  doi: 10.1111/febs.16351
– ident: e_1_2_11_8_1
  doi: 10.1161/CIRCRESAHA.111.247866
– ident: e_1_2_11_25_1
  doi: 10.1016/S0022-2828(03)00084-1
– ident: e_1_2_11_41_1
  doi: 10.1038/s41417‐019‐0109‐7
– ident: e_1_2_11_44_1
  doi: 10.1161/CIRCULATIONAHA.117.031358
– ident: e_1_2_11_33_1
  doi: 10.3390/ijms22052245
– ident: e_1_2_11_13_1
  doi: 10.1038/nature20099
– ident: e_1_2_11_4_1
  doi: 10.15252/embj.2018100492
– ident: e_1_2_11_9_1
  doi: 10.1016/j.devcel.2019.10.007
– ident: e_1_2_11_31_1
  doi: 10.1111/acel.12811
– ident: e_1_2_11_6_1
  doi: 10.1038/nature16932
– ident: e_1_2_11_17_1
  doi: 10.1172/JCI162519
– ident: e_1_2_11_47_1
  doi: 10.1016/j.bbrc.2013.03.097
– ident: e_1_2_11_28_1
  doi: 10.1016/j.phrs.2022.106356
– ident: e_1_2_11_21_1
  doi: 10.1097/FJC.0000000000000878
– ident: e_1_2_11_51_1
  doi: 10.1111/acel.13753
– ident: e_1_2_11_36_1
  doi: 10.1042/EBC20170022
– ident: e_1_2_11_34_1
  doi: 10.1038/s41569‐021‐00624‐2
– ident: e_1_2_11_38_1
  doi: 10.1016/j.mad.2021.111540
– ident: e_1_2_11_30_1
  doi: 10.1016/j.jaccao.2023.03.012
– ident: e_1_2_11_16_1
  doi: 10.1074/jbc.M210640200
– ident: e_1_2_11_40_1
  doi: 10.1016/s0008‐6363(02)00660‐0
– ident: e_1_2_11_29_1
  doi: 10.1111/acel.12931
– ident: e_1_2_11_56_1
  doi: 10.3389/fgene.2013.00024
– ident: e_1_2_11_32_1
  doi: 10.1111/acel.13015
– ident: e_1_2_11_39_1
  doi: 10.1016/j.jacbts.2017.12.006
– ident: e_1_2_11_3_1
  doi: 10.1126/scisignal.abn8017
– ident: e_1_2_11_45_1
  doi: 10.1016/j.cell.2017.02.004
– ident: e_1_2_11_43_1
  doi: 10.1016/j.mad.2022.111740
– ident: e_1_2_11_18_1
  doi: 10.1007/s00441‐006‐0324‐z
– ident: e_1_2_11_46_1
  doi: 10.1038/nrc3960
– ident: e_1_2_11_50_1
  doi: 10.1128/MCB.21.10.3375‐3386.2001
– ident: e_1_2_11_27_1
  doi: 10.1093/eurjhf/hft028
– ident: e_1_2_11_11_1
  doi: 10.1161/CIRCULATIONAHA.121.054204
– ident: e_1_2_11_22_1
  doi: 10.1089/ars.2012.4616
– ident: e_1_2_11_10_1
  doi: 10.15252/emmm.202013792
– ident: e_1_2_11_52_1
  doi: 10.1038/s41586‐020‐2496‐1
– ident: e_1_2_11_53_1
  doi: 10.4161/auto.6.5.11947
– ident: e_1_2_11_12_1
  doi: 10.1158/2159‐8290.CD‐16‐0241
– ident: e_1_2_11_37_1
  doi: 10.1016/j.bbrc.2007.01.089
– ident: e_1_2_11_55_1
  doi: 10.1111/acel.12945
– ident: e_1_2_11_7_1
  doi: 10.1080/10985549.2023.2229225
– ident: e_1_2_11_15_1
  doi: 10.1177/1933719117737842
– ident: e_1_2_11_24_1
  doi: 10.1172/JCI22475
– ident: e_1_2_11_54_1
  doi: 10.15420/cfr.2022.06
– ident: e_1_2_11_14_1
  doi: 10.1111/acel.13249
– ident: e_1_2_11_23_1
  doi: 10.1161/CIRCRESAHA.109.198366
– ident: e_1_2_11_26_1
  doi: 10.1016/j.ceb.2017.02.014
– ident: e_1_2_11_35_1
  doi: 10.1016/j.yjmcc.2011.07.019
– ident: e_1_2_11_57_1
  doi: 10.1111/acel.12344
– ident: e_1_2_11_42_1
  doi: 10.1038/nature09787
– ident: e_1_2_11_20_1
  doi: 10.1161/CIRCULATIONAHA.109.871137
– ident: e_1_2_11_2_1
  doi: 10.1038/s41569‐023‐00881‐3
SSID ssj0017903
Score 2.451079
Snippet The aging heart is characterized by a number of structural changes leading to ventricular stiffness, impaired resistance to stress and increased risk of...
SourceID pubmedcentral
hal
proquest
pubmed
crossref
wiley
SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage e14204
SubjectTerms AC133 Antigen - genetics
AC133 Antigen - metabolism
Aging
Aging - genetics
Aging - metabolism
Aging - physiology
Animals
Biochemistry, Molecular Biology
Cardiology and cardiovascular system
cardiomyocyte
Cardiomyocytes
Cardiomyopathy
Cardiovascular disease
Cell cycle
Cellular Senescence - genetics
Congestive heart failure
Coronary artery disease
Cytokines
Cytotoxicity
DNA damage
Doxorubicin
Ejection fraction
Fibrosis
Genomics
heart
Heart diseases
Heart failure
Heart Failure - genetics
Heart Failure - metabolism
Heart Failure - pathology
Human health and pathology
Humans
Hypertrophy
Ischemia
Kinases
Laboratory animals
Life Sciences
Male
Mice
Mice, Inbred C57BL
Myocytes, Cardiac - metabolism
Oxidative stress
p53 Protein
Senescence
Surgery
Telomeres
Transcriptomics
SummonAdditionalLinks – databaseName: ProQuest Central
  dbid: BENPR
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3NatwwEB6aDYVeQtNfN0lRf04FU1nWau1T2YYNS0lDKA3kUowkSySQ2pvsprC3PEKfMU-SGVnedgkEX4QlbGvGGn3SjL4B-Igmj7xrQxxpjtyMZAdLLVJZGm9Gta69pNPI34_U9ER-Ox2exg23eQyr7G1iMNR1a2mP_HNO3GU5TjD8y-wypaxR5F2NKTQ2YBNNcFEMYPPr5Oj4x8qPMCpDbuRMjmRaohmOBKUUy6Otu0A7IWKKtn5K2jijgMj7aPN-0OT_YDbMRgdPYSvCSDbu9L4Nj1zzDB53iSWXz-FXd_7Wxw051np2fNUSjUhze_NXMD1nmiGgZrMLjZib6m0ITP29bO1y4dicTKClUc_OG4YgkYVsRozyXy9ewMnB5Of-NI2JFFIrpZBprQo6UyotN1wJbrLMIDJQpcei4nnJvdGlM8qrPLOqlnUpuR5mGi9sZHj-EgZN27jXwHBKHznrBa6SrPQmI3IZZXhtuBGF83kCH3pZVrOOL6Pq1xkk8SpIPIH3KOZVA6K4no4PK7pHBPC4hpJ_sgR2ey1UcWDNq3-_QQLvVtU4JMjPoRvXXmMbBHUIpAqBj3jVKW31qpwI_BEVJVCsqXPtW9ZrmvOzQLtNK8cil9jFT0HzD_SvGu9PDkPpzcOd2IEnAkXaBa3twmBxde32EOUszNv4K98Bev_6cQ
  priority: 102
  providerName: ProQuest
– databaseName: Wiley Online Library - Core collection (SURFmarket)
  dbid: DR2
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1La9wwEB7SQKGXPpI-nKZFTXsqOMiyVmtDL0tIWEIaQmkgl2AkWSKhqR2y3sD21J_Q39hf0hn50WwCgRZfhCU_9JjRJ2nmG4APqPLodG2EkubomJH0YK5FLHPjzbjUpZfkjfz5UE2P5f7J6GQFPvW-MC0_xLDhRpIR9DUJuDazG0KurbtAOReBDJSMtQgRfRm4o4h5KljXy7GMc9TAHTcpmfH8fXRpNnpwRraQd4HmXXvJmzg2TER7T-C0r0Jrf_Jte96YbfvjFrvj_9bxKTzuECqbtEPqGay4ag0etjErF-tw2rr2-m6vj9WeHV3VxFBS_f75SzA9Y5ohVmeXFxrhPOXbYPP6fVHbRePYjLSrJYXCziuG-JOFQEmMQms3z-F4b_frzjTuYjTEVkoh41Jl5K4qLTdcCW6SxCDoULnHpOJpzr3RuTPKqzSxqpRlLrkeJRovLGR4-gJWq7pyr4AhWhg76wUuwKz0JiHeGmV4abgRmfNpBO_7viouWyqOol_CUEMVoaEi2MJuHAoQe_Z0clDQPeKWx-WZvE4i2Ox7uehkdlakxI6XIoThEbwbslHa6AhFV66eYxnEi4jRMoGveNkOiuFTKcUGQMAVQbY0XJb-ZTmnOj8LjN60KM1SiVX8GIbDPfUrJju7ByG18S-FX8MjgQ3cWsdtwmpzNXdvEE415m0Qmz-nLxpX
  priority: 102
  providerName: Wiley-Blackwell
Title Identification of Prominin‐2 as a new player of cardiomyocyte senescence in the aging heart
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Facel.14204
https://www.ncbi.nlm.nih.gov/pubmed/38757782
https://www.proquest.com/docview/3117932380
https://www.proquest.com/docview/3056663821
https://hal.science/hal-04618754
https://pubmed.ncbi.nlm.nih.gov/PMC11488343
Volume 23
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1La9wwEB7yoCWX0mfqNl3Ux6ngIsta2T6Usg0blpKEJXQhl2IkWyKBrZ3ubkr31p_Q39hf0hnZ3tak9FAMxliyZc94Rp-s0TcAr9Dl0ezaEC3N0jQj-cFMi1Bmxpmk1KWTtBr55FRNZvLD-fB8C7r8na0Al38d2lE-qdli_ubbl_U7NPi3XVSOLuwcLV4QLegu9kgJZTI4kb9nE5LMZ0iOZCLDDJ1xS1Pav3YPbsfE7p6kotdHbV9QhORN-HkzivJPdOu7p6O7cKfFlWzUfAj3YMtW9-FWk2ly_QA-NQtyXfuHjtWOTRc18YpUP7__EEwvmWaIsNnVXCMIp_LCR6p-XtfFemXZknxiQW6AXVYMUSPz6Y0YJcRePYTZ0fjj4SRsMyuEhZRChqVKaZGpLLjhSnATRQahgsocHioeZ9wZnVmjnIqjQpWyzCTXw0jjhpUMjx_BTlVX9jEw7OMTWziBw6ZCOhMR24wyvDTciNS6OICXnSzzq4ZAI-8GHiT83As_gBco5k0F4ryejI5zOkeM8KgX-TUK4KDTQt59KHlMnHYxAg8ewPNNMdoITXzoytbXWAdRHiKrVOAt9hulbZrqdB5A2lNn71n6JdXlhefhpqFkGkt8xdde8_94v3x0OD72R0_-v52nsCdQ3E2E2wHsrBbX9hlCopUZwLaQ0wHsvh-fTs8G_scC7c_EwFvCL70iDRM
linkProvider Scholars Portal
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV3NbhMxEB61qRC9IP5ZKGD-LkgrvF7H2T0gFEqqlKZRhVqpl2qxvbZaqd0NTQrKjUfgSXgonoSZ_QlElXqrclnFlhPP2ONvdsbzAbxGk0fRtS7uNEdhRrKDqRahTI03vVznXtJt5N2xGh7Iz4fdwxX43d6FobTK1iZWhjovLb0jfxdT7bIYDxj-YfItJNYoiq62FBr1sthx8x_osk3fb39C_b4RYmuwvzkMG1aB0EopZJirhC5YSssNV4KbKDJ4TKrU46Piccq90akzyqs4siqXeSq57kYaP9jJ8BjHXYU1GSsuOrD2cTDe-7KIW_TSios5wvHDFM1-UxCVcoe0dadol0RDCdcegavHlIB5Gd1eTtL8HzxXp9_WbbjVwFbWr9fZHVhxxV24URNZzu_BUX3f1zcvAFnp2d55SWVLij8_fwmmp0wzBPBscqoR41O7rRJhz-alnc8cm5LJtWRl2EnBEJSyij2JEd_27D4cXIuIH0CnKAv3CBhCiJ6zXqBXZqU3ERWzUYbnhhuROB8H8KqVZTap63NkrV9DEs8qiQfwEsW86EAltYf9UUbfUcF59Nnk9yiAjVYLWbORp9m_ZRfAi0UzbkGKq-jClRfYB0EkArdE4BAPa6UtfiomwgBEYQEkS-pc-i_LLcXJcVXmmzzVJJY4xbeV5q-YX9bfHIyqp8dXT-I53Bzu746y0fZ45wmsCxRvnTC3AZ3Z-YV7ighrZp41y5rB1-veSX8Be6w1QQ
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1fa9swED_alJW9jK1bN6_dpv15GhhkWVFs2EvoGrItLX1YRhkMI8kSLXR2aNJB3vYR-hn3SXYnO15DYVD8Iiz5353v9JN0-h3AO3R5tLrWR0tztMxIfjDXIpa58WZQ6tJL2o18dKzGU_n5tH-6AR9We2Eafohuwo0sI_hrMvBZ6W8YubbuAu1cEBnoVh-7Jd6DreG36fdpt4owyENm5EQOZJyjE27pSSmS59_Vax3S5hmFQ97GmrdDJm9C2dAXjR7CgxZEsmGj9Uew4aoduNeklVw-hh_N7lvfTsex2rOTy5pIRKo_v68F03OmGcJpNrvQiLip3oaw1J_L2i4Xjs3JAVqyeXZeMYSILOQyYpT9evEEpqPDrwfjuE2jEFsphYxLldGOUmm54UpwkyQGcYHKPRYVT3Pujc6dUV6liVWlLHPJdT_ReGAjw9Nd6FV15Z4Bww594KwXOEay0puEqGWU4aXhRmTOpxG8XcmymDVsGcVqlEESL4LEI3iDYu4aEMH1eDgp6BzRv-MISv5KIthfaaFozWpepERglyLK4BG87qrRIGiVQ1euvsI2COkQRmUCb_G0UVr3qJTo-xETRZCtqXPtXdZrqvOzQLpN48YslfiJ74Pm__N9xfDgcBJKz-_S-BVsn3wcFZNPx1_24L5AWTexbPvQW1xeuRcIfhbmZfuP_wUfKf5N
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Identification+of+Prominin%E2%80%902+as+a+new+player+of+cardiomyocyte+senescence+in+the+aging+heart&rft.jtitle=Aging+cell&rft.au=Maggiorani%2C+D.&rft.au=Santin%2C+Y.&rft.au=Formoso%2C+K.&rft.au=Drap%C3%A9%2C+E.&rft.date=2024-09-01&rft.pub=John+Wiley+and+Sons+Inc&rft.issn=1474-9718&rft.eissn=1474-9726&rft.volume=23&rft.issue=9&rft_id=info:doi/10.1111%2Facel.14204&rft_id=info%3Apmid%2F38757782&rft.externalDocID=PMC11488343
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1474-9718&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1474-9718&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1474-9718&client=summon