Cellular Senescence and Regulated Cell Death of Tubular Epithelial Cells in Diabetic Kidney Disease

Cellular senescence is frequently evident at etiologic sites of chronic diseases and involves essentially irreversible arrest of cell proliferation, increased protein production, resistance to apoptosis, and altered metabolic activity. Regulated cell death plays a vital role in shaping fully functio...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in endocrinology (Lausanne) Vol. 13; p. 924299
Main Authors Shen, Shuang, Ji, Chuanyuan, Wei, Kaifeng
Format Journal Article
LanguageEnglish
Published Frontiers Media S.A 28.06.2022
Subjects
Online AccessGet full text

Cover

Loading…
Abstract Cellular senescence is frequently evident at etiologic sites of chronic diseases and involves essentially irreversible arrest of cell proliferation, increased protein production, resistance to apoptosis, and altered metabolic activity. Regulated cell death plays a vital role in shaping fully functional organs during the developmental process, coordinating adaptive or non-adaptive responses, and coping with long-term harmful intracellular or extracellular homeostasis disturbances. In recent years, the concept of ‘diabetic tubulopathy’ has emerged. tubular epithelial cells are particularly susceptible to the derangements of diabetic state because of the virtue of the high energy requirements and reliance on aerobic metabolism render. Hyperglycemia, oxidative stress, persistent chronic inflammation, glucose toxicity, advanced glycation end-products (AGEs) accumulation, lipid metabolism disorders, and lipotoxicity contribute to the cellular senescence and different patterns of regulated cell death (apoptosis, autophagic cell death, necroptosis, pyroptosis, and ferroptosis) in tubular epithelial cells. We now explore the ‘tubulocentric’ view of diabetic kidney disease(DKD). And we summarize recent discoveries regarding the development and regulatory mechanisms of cellular senescence, apoptosis, autophagic cell death, necroptosis, pyroptosis, and ferroptosis in the pathogenesis of DKD. These findings provide new perspectives on the mechanisms of DKD and are useful for designing novel therapeutic approaches for the treatment of DKD.
AbstractList Cellular senescence is frequently evident at etiologic sites of chronic diseases and involves essentially irreversible arrest of cell proliferation, increased protein production, resistance to apoptosis, and altered metabolic activity. Regulated cell death plays a vital role in shaping fully functional organs during the developmental process, coordinating adaptive or non-adaptive responses, and coping with long-term harmful intracellular or extracellular homeostasis disturbances. In recent years, the concept of ‘diabetic tubulopathy’ has emerged. tubular epithelial cells are particularly susceptible to the derangements of diabetic state because of the virtue of the high energy requirements and reliance on aerobic metabolism render. Hyperglycemia, oxidative stress, persistent chronic inflammation, glucose toxicity, advanced glycation end-products (AGEs) accumulation, lipid metabolism disorders, and lipotoxicity contribute to the cellular senescence and different patterns of regulated cell death (apoptosis, autophagic cell death, necroptosis, pyroptosis, and ferroptosis) in tubular epithelial cells. We now explore the ‘tubulocentric’ view of diabetic kidney disease(DKD). And we summarize recent discoveries regarding the development and regulatory mechanisms of cellular senescence, apoptosis, autophagic cell death, necroptosis, pyroptosis, and ferroptosis in the pathogenesis of DKD. These findings provide new perspectives on the mechanisms of DKD and are useful for designing novel therapeutic approaches for the treatment of DKD.
Cellular senescence is frequently evident at etiologic sites of chronic diseases and involves essentially irreversible arrest of cell proliferation, increased protein production, resistance to apoptosis, and altered metabolic activity. Regulated cell death plays a vital role in shaping fully functional organs during the developmental process, coordinating adaptive or non-adaptive responses, and coping with long-term harmful intracellular or extracellular homeostasis disturbances. In recent years, the concept of 'diabetic tubulopathy' has emerged. tubular epithelial cells are particularly susceptible to the derangements of diabetic state because of the virtue of the high energy requirements and reliance on aerobic metabolism render. Hyperglycemia, oxidative stress, persistent chronic inflammation, glucose toxicity, advanced glycation end-products (AGEs) accumulation, lipid metabolism disorders, and lipotoxicity contribute to the cellular senescence and different patterns of regulated cell death (apoptosis, autophagic cell death, necroptosis, pyroptosis, and ferroptosis) in tubular epithelial cells. We now explore the 'tubulocentric' view of diabetic kidney disease(DKD). And we summarize recent discoveries regarding the development and regulatory mechanisms of cellular senescence, apoptosis, autophagic cell death, necroptosis, pyroptosis, and ferroptosis in the pathogenesis of DKD. These findings provide new perspectives on the mechanisms of DKD and are useful for designing novel therapeutic approaches for the treatment of DKD.Cellular senescence is frequently evident at etiologic sites of chronic diseases and involves essentially irreversible arrest of cell proliferation, increased protein production, resistance to apoptosis, and altered metabolic activity. Regulated cell death plays a vital role in shaping fully functional organs during the developmental process, coordinating adaptive or non-adaptive responses, and coping with long-term harmful intracellular or extracellular homeostasis disturbances. In recent years, the concept of 'diabetic tubulopathy' has emerged. tubular epithelial cells are particularly susceptible to the derangements of diabetic state because of the virtue of the high energy requirements and reliance on aerobic metabolism render. Hyperglycemia, oxidative stress, persistent chronic inflammation, glucose toxicity, advanced glycation end-products (AGEs) accumulation, lipid metabolism disorders, and lipotoxicity contribute to the cellular senescence and different patterns of regulated cell death (apoptosis, autophagic cell death, necroptosis, pyroptosis, and ferroptosis) in tubular epithelial cells. We now explore the 'tubulocentric' view of diabetic kidney disease(DKD). And we summarize recent discoveries regarding the development and regulatory mechanisms of cellular senescence, apoptosis, autophagic cell death, necroptosis, pyroptosis, and ferroptosis in the pathogenesis of DKD. These findings provide new perspectives on the mechanisms of DKD and are useful for designing novel therapeutic approaches for the treatment of DKD.
Author Shen, Shuang
Ji, Chuanyuan
Wei, Kaifeng
AuthorAffiliation College of Traditional Chinese Medicine·College of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine , Nanjing , China
AuthorAffiliation_xml – name: College of Traditional Chinese Medicine·College of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine , Nanjing , China
Author_xml – sequence: 1
  givenname: Shuang
  surname: Shen
  fullname: Shen, Shuang
– sequence: 2
  givenname: Chuanyuan
  surname: Ji
  fullname: Ji, Chuanyuan
– sequence: 3
  givenname: Kaifeng
  surname: Wei
  fullname: Wei, Kaifeng
BookMark eNp1kU9vEzEQxS1UREvpB-DmI5cEr727ti9IKC1tRSUkKGdrbM8mrhw7rDeV-u3xJkWiSPjgP-P3fhrNe0tOUk5IyPuGLYVQ-uOAyeclZ5wvNW-51q_IWdP37YILzU_-up-Si1IeWF0ta7RWb8ip6JSQXMsz4lYY4z7CSH9gwuIwOaSQPP2O61qe0NNZQS8Rpg3NA73f24P8ahemDcYA8SAoNCR6GcDiFBz9GnzCp_ouCAXfkdcDxIIXz-c5-fnl6n51s7j7dn27-ny3cB1T00ILxTvHvGu8Ayms5G0HneKcWduwQaKVzoIVyjFm6zZ0yLDthdXMddyjOCe3R67P8GB2Y9jC-GQyBHMo5HFtYKztRTRSAddedUr6vh38YHvBBNhGDk4Lr6GyPh1Zu73doq9zmUaIL6Avf1LYmHV-NJpLIUVfAR-eAWP-tccymW2o440REuZ9MbzXDWulamepPErdmEsZcTAuTDCFPJNDNA0zc-LmkLiZEzfHxKuz-cf5p8H_e34DsAixeA
CitedBy_id crossref_primary_10_1007_s40618_023_02267_1
crossref_primary_10_1016_j_jep_2023_117354
crossref_primary_10_18499_2225_7357_2023_12_4_38_46
crossref_primary_10_1016_j_intimp_2024_113236
crossref_primary_10_1038_s41598_023_43411_4
crossref_primary_10_3390_ijms241713502
crossref_primary_10_1002_adtp_202300379
crossref_primary_10_1016_j_jcte_2025_100387
crossref_primary_10_1186_s12882_024_03931_1
crossref_primary_10_1016_j_ejphar_2024_176699
crossref_primary_10_3389_fphar_2024_1508312
crossref_primary_10_3390_genes14030609
crossref_primary_10_1016_j_heliyon_2024_e24872
crossref_primary_10_1016_j_lfs_2023_122108
crossref_primary_10_3389_fphar_2024_1379821
crossref_primary_10_1016_j_bcp_2024_116642
crossref_primary_10_3389_fendo_2023_1232790
crossref_primary_10_1016_j_trsl_2023_11_002
crossref_primary_10_18632_aging_205405
crossref_primary_10_3390_antiox13060675
crossref_primary_10_3390_ijms24032133
crossref_primary_10_1002_ptr_7993
crossref_primary_10_2174_0113892010276372231129105022
crossref_primary_10_4103_aja202331
crossref_primary_10_1038_s41419_024_06833_0
crossref_primary_10_1016_j_cbi_2023_110640
crossref_primary_10_1080_0886022X_2023_2292753
crossref_primary_10_2147_DMSO_S450695
crossref_primary_10_1155_2022_5040458
crossref_primary_10_2147_JIR_S435596
crossref_primary_10_1172_jci_insight_178373
crossref_primary_10_1016_j_intimp_2024_112138
crossref_primary_10_1089_ars_2024_0575
crossref_primary_10_1186_s10020_024_00824_9
crossref_primary_10_1016_j_phymed_2025_156411
crossref_primary_10_1016_j_biopha_2023_114897
crossref_primary_10_1016_j_intimp_2024_112131
crossref_primary_10_3390_molecules27196221
crossref_primary_10_1080_13880209_2024_2314705
crossref_primary_10_1016_j_bbrc_2024_149744
crossref_primary_10_1016_j_scitotenv_2025_178852
crossref_primary_10_3390_nu15184050
crossref_primary_10_3389_fcell_2023_1271145
crossref_primary_10_3389_fnmol_2023_1113081
crossref_primary_10_1159_000529995
crossref_primary_10_1002_jex2_70038
crossref_primary_10_18632_aging_205233
Cites_doi 10.2337/dc12-0849
10.1016/j.molcel.2014.10.021
10.1681/ASN.2005070776
10.1186/gb-2013-14-10-r115
10.1111/imr.12295
10.1038/nature05315
10.1038/nature09663
10.1038/ncb1482
10.1098/rsbl.2017.0463
10.1016/j.cell.2010.07.018
10.1016/S0092-8674(01)00492-5
10.1016/j.cell.2010.01.028
10.1371/journal.pone.0038285
10.1152/ajpcell.00096.2014
10.1007/s00125-017-4490-1
10.15252/embr.201439496
10.1126/science.1172308
10.1016/j.ajpath.2016.12.011
10.1172/JCI111523
10.3390/ijms17060975
10.1681/ASN.2017050574
10.1146/annurev-immunol-032414-112248
10.1371/journal.pone.0041831
10.1016/j.jdiacomp.2015.07.021
10.1038/s41580-020-0270-8
10.1371/journal.pone.0228385
10.1007/s00018-016-2203-4
10.1016/S2213-8587(19)30160-3
10.2337/diabetes.49.3.466
10.1038/ng.2363
10.1002/jcp.10119
10.1016/j.cardiores.2004.05.001
10.1038/nature14879
10.1038/aps.2015.21
10.3389/fendo.2021.626390
10.1038/sj.emboj.7601689
10.1016/j.bbrc.2014.11.075
10.1038/nature13706
10.1111/j.1365-2796.2009.02139.x
10.4049/jimmunol.1201959
10.1172/jci.insight.96968
10.1016/j.freeradbiomed.2020.10.323
10.1016/j.freeradbiomed.2016.04.013
10.1016/j.ejphar.2020.173574
10.1038/embor.2012.19
10.2741/1853
10.1038/nm.3386
10.1126/science.1249361
10.1038/labinvest.2011.93
10.1038/nrm2153
10.1152/ajpregu.00809.2010
10.1038/nrdp.2015.18
10.1038/s41419-021-03452-x
10.1371/journal.pone.0039586
10.1093/ndt/gfn351
10.1371/journal.pone.0125176
10.1172/JCI26390
10.2215/CJN.11111016
10.1007/s00441-017-2588-x
10.1016/j.jdiacomp.2014.05.010
10.1681/ASN.2014050457
10.2337/db16-0796
10.1080/15548627.2016.1187366
10.7554/eLife.30543
10.1016/j.freeradbiomed.2018.09.008
10.1007/s40620-020-00868-0
10.2337/db15-0384
10.1038/cdd.2009.121
10.1681/ASN.2008050503
10.1172/JCI69557
10.1164/rccm.201510-2106CI
10.1038/ni.3015
10.4049/jimmunol.1100613
10.1038/nsmb.3319
10.3390/ph12010026
10.1007/s00125-006-0322-4
10.1172/jci.insight.98720
10.1152/ajprenal.00164.2016
10.1038/nm.3363
10.1056/NEJM199811123392007
10.1016/j.chembiol.2020.02.005
10.1080/15548627.2020.1824694
10.1155/2019/7495629
10.1093/ndt/gfv264
10.1016/j.molmet.2019.10.005
10.1038/nrm2529
10.1038/ncomms7282
10.1016/j.cell.2017.09.021
10.1038/s41422-019-0164-5
10.1101/gad.1787609
10.1096/fj.09-152488
10.3389/fphar.2014.00117
10.1038/cddis.2009.16
ContentType Journal Article
Copyright Copyright © 2022 Shen, Ji and Wei.
Copyright © 2022 Shen, Ji and Wei 2022 Shen, Ji and Wei
Copyright_xml – notice: Copyright © 2022 Shen, Ji and Wei.
– notice: Copyright © 2022 Shen, Ji and Wei 2022 Shen, Ji and Wei
DBID AAYXX
CITATION
7X8
5PM
DOA
DOI 10.3389/fendo.2022.924299
DatabaseName CrossRef
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ Directory of Open Access Journals
DatabaseTitle CrossRef
MEDLINE - Academic
DatabaseTitleList

MEDLINE - Academic
CrossRef
Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 1664-2392
ExternalDocumentID oai_doaj_org_article_78a29d8587d64fdfb6303ab17fc93d9a
PMC9273736
10_3389_fendo_2022_924299
GroupedDBID 53G
5VS
9T4
AAFWJ
AAKDD
AAYXX
ACGFO
ACGFS
ACXDI
ADBBV
ADRAZ
AFPKN
ALMA_UNASSIGNED_HOLDINGS
AOIJS
BAWUL
BCNDV
CITATION
DIK
EMOBN
GROUPED_DOAJ
GX1
HYE
KQ8
M48
M~E
OK1
PGMZT
RPM
7X8
5PM
ID FETCH-LOGICAL-c508t-93825c0dc1dca73b7245a58220bb10f7eb7cbab38c00b8c0f5e0e463b90c52de3
IEDL.DBID DOA
ISSN 1664-2392
IngestDate Wed Aug 27 01:23:39 EDT 2025
Thu Aug 21 14:00:50 EDT 2025
Fri Jul 11 02:45:47 EDT 2025
Tue Jul 01 04:28:05 EDT 2025
Thu Apr 24 22:56:41 EDT 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Language English
License This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c508t-93825c0dc1dca73b7245a58220bb10f7eb7cbab38c00b8c0f5e0e463b90c52de3
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
This article was submitted to Renal Endocrinology, a section of the journal Frontiers in Endocrinology
Edited by: Jun Wada, Okayama University, Japan
Reviewed by: Fan Yang, Jiangxi Agricultural University, China; Hitoshi Sugiyama, Kawasaki Medical University General Hospital, Japan
OpenAccessLink https://doaj.org/article/78a29d8587d64fdfb6303ab17fc93d9a
PMID 35837297
PQID 2691047846
PQPubID 23479
ParticipantIDs doaj_primary_oai_doaj_org_article_78a29d8587d64fdfb6303ab17fc93d9a
pubmedcentral_primary_oai_pubmedcentral_nih_gov_9273736
proquest_miscellaneous_2691047846
crossref_citationtrail_10_3389_fendo_2022_924299
crossref_primary_10_3389_fendo_2022_924299
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2022-06-28
PublicationDateYYYYMMDD 2022-06-28
PublicationDate_xml – month: 06
  year: 2022
  text: 2022-06-28
  day: 28
PublicationDecade 2020
PublicationTitle Frontiers in endocrinology (Lausanne)
PublicationYear 2022
Publisher Frontiers Media S.A
Publisher_xml – name: Frontiers Media S.A
References Epstein (B2) 1998; 339
Thomas (B3) 2015; 1
Martindale (B43) 2002; 192
Wanner (B30) 2017; 369
Keating (B29) 2018; 61
Moriwaki (B56) 2016; 73
Chevalier (B9) 2016; 311
Riedl (B42) 2007; 8
Wang (B73) 2020; 888
Dos hi (B1) 2017; 12
KK (B19) 2014; 28
Xiong (B4) 2019; 2019
Tang (B5) 2019; 29
Liu (B21) 2015; 308
Zhou (B69) 2011; 469
Wang (B93) 2014; 15
Matsuzawa (B85) 2015; 456
Kim (B74) 2021; 12
Feng (B76) 2021; 12
Luo (B37) 2018; 29
Stockwell (B75) 2017; 171
Wirawan (B80) 2010; 1
Bauernfeind (B65) 2011; 187
Hasegawa (B15) 2013; 19
Kose (B70) 2019; 12
Lawlor (B59) 2015; 6
Kevin (B83) 2012; 7
Lovshin (B62) 2018; 3
Reichert (B25) 2017; 13
Mauer (B8) 1984; 74
Sampson (B23) 2006; 49
Yu (B51) 2021; 34
Basuli (B71) 2014; 5
Li (B77) 2021; 162
Kim (B17) 2013; 36
Gilbert (B11) 2017; 66
Horvath (B33) 2013; 14
Galluzzi (B57) 2012; 13
Wang (B67) 2013; 190
Ghosh (B88) 2012; 7
Fyhrquist (B24) 2009; 267
Liu (B86) 2020; 27
Wang (B68) 2012; 7
Blackburn (B22) 2001; 106
Wu (B38) 2011; 91
Cassis (B52) 2018; 3
Jennifer (B7) 2015; 30
Zhan (B40) 2015; 26
Karch (B46) 2017; 6
Nihalani (B16) 2013; 19
Wauer (B34) 2015; 524
Yousefi (B82) 2006; 8
Takahashi (B89) 2014; 513
Zhang (B20) 2006; 17
Sassy-Prigent (B64) 2000; 49
Nunzia D'Onofrio (B18) 2016; 96
Preiss (B50) 2019; 7
Moreno-Gonzalez (B58) 2016; 194
Mizushima (B48) 2010; 140
Wang (B66) 2015; 36
Fu (B12) 2019; 30
Vallon (B10) 2011; 300
Bedoui (B6) 2020; 21
Zhu (B60) 2020; 15
Ohnishi (B36) 2010; 24
Kroemer (B45) 2008; 9
Fouquerel (B26) 2016; 23
Tesch (B44) 2015; 64
Xu (B54) 2015; 29
Lans (B27) 2012; 44
Yonekawa (B84) 2015; 16
Stoyanovsky (B72) 2019; 133
Maiuri (B78) 2007; 26
Luo (B79) 2010; 17
Zhang (B90) 2009; 325
White (B14) 2008; 23
Russo (B13) 2009; 20
Goldberg (B39) 2015; 265
Urakawa (B35) 2006; 444
Radoshevich (B81) 2010; 142
Mandal (B92) 2014; 56
Newton (B91) 2014; 343
Hayashi (B31) 2014; 124
Giuseppina (B63) 2004; 63
Hou (B87) 2016; 12
Berger (B28) 2009; 23
Sharma (B32) 2017; 187
Levine (B47) 2005; 115
Guo (B41) 2015; 10
Moto (B49) 2016; 17
Yang (B53) 2020; 17
Chan (B55) 2015; 33
Sharma (B61) 2006; 11
References_xml – volume: 36
  year: 2013
  ident: B17
  article-title: Urinary Cystatin C and Tubular Proteinuria Predict Progression of Diabetic Nephropathy
  publication-title: Diabetes Care
  doi: 10.2337/dc12-0849
– volume: 56
  year: 2014
  ident: B92
  article-title: RIP3 Induces Apoptosis Independent of Pronecrotic Kinase Activity
  publication-title: Mol Cell
  doi: 10.1016/j.molcel.2014.10.021
– volume: 17
  year: 2006
  ident: B20
  article-title: Downregulation of Connexin 43 Expression by High Glucose Induces Senescence in Glomerular Mesangial Cells
  publication-title: J Am Soc Nephrol
  doi: 10.1681/ASN.2005070776
– volume: 14
  year: 2013
  ident: B33
  article-title: DNA Methylation Age of Human Tissues and Cell Types
  publication-title: Genome Biol
  doi: 10.1186/gb-2013-14-10-r115
– volume: 265
  start-page: 63
  year: 2015
  ident: B39
  article-title: Drivers of Age-Related Inflammation and Strategies for Healthspan Extension
  publication-title: Immunol Rev
  doi: 10.1111/imr.12295
– volume: 444
  year: 2006
  ident: B35
  article-title: Klotho Converts Canonical FGF Receptor Into a Specific Receptor for FGF23
  publication-title: Nature
  doi: 10.1038/nature05315
– volume: 469
  year: 2011
  ident: B69
  article-title: A Role for Mitochondria in NLRP3 Inflammasome Activation
  publication-title: Nature
  doi: 10.1038/nature09663
– volume: 8
  year: 2006
  ident: B82
  article-title: Calpain-Mediated Cleavage of Atg5 Switches Autophagy to Apoptosis
  publication-title: Nat Cell Biol
  doi: 10.1038/ncb1482
– volume: 13
  start-page: 20170463
  year: 2017
  ident: B25
  article-title: Does Oxidative Stress Shorten Telomeres In Vivo? A Review
  publication-title: Biol Lett
  doi: 10.1098/rsbl.2017.0463
– volume: 142
  start-page: 590
  year: 2010
  ident: B81
  article-title: ATG12 Conjugation to ATG3 Regulates Mitochondrial Homeostasis and Cell Death
  publication-title: Cell
  doi: 10.1016/j.cell.2010.07.018
– volume: 106
  year: 2001
  ident: B22
  article-title: Switching and Signaling at the Telomere
  publication-title: Cell
  doi: 10.1016/S0092-8674(01)00492-5
– volume: 140
  year: 2010
  ident: B48
  article-title: Methods in Mammalian Autophagy Research
  publication-title: Cell
  doi: 10.1016/j.cell.2010.01.028
– volume: 7
  year: 2012
  ident: B68
  article-title: Quercetin and Allopurinol Ameliorate Kidney Injury in STZ-Treated Rats With Regulation of Renal NLRP3 Inflammasome Activation and Lipid Accumulation
  publication-title: PloS One
  doi: 10.1371/journal.pone.0038285
– volume: 308
  year: 2015
  ident: B21
  article-title: Impact of ER Stress-Regulated ATF4/p16 Signaling on the Premature Senescence of Renal Tubular Epithelial Cells in Diabetic Nephropathy
  publication-title: Am J Physiol Cell Physiol
  doi: 10.1152/ajpcell.00096.2014
– volume: 61
  start-page: 6
  year: 2018
  ident: B29
  article-title: Epigenetics in Diabetic Nephropathy, Immunity and Metabolism
  publication-title: Diabetologia
  doi: 10.1007/s00125-017-4490-1
– volume: 16
  year: 2015
  ident: B84
  article-title: RIP1 Negatively Regulates Basal Autophagic Flux Through TFEB to Control Sensitivity to Apoptosis
  publication-title: EMBO Rep
  doi: 10.15252/embr.201439496
– volume: 325
  year: 2009
  ident: B90
  article-title: RIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death From Apoptosis to Necrosis
  publication-title: Science
  doi: 10.1126/science.1172308
– volume: 187
  year: 2017
  ident: B32
  article-title: High Glucose-Induced Hypomethylation Promotes Binding of Sp-1 to Myo-Inositol Oxygenase
  publication-title: Am J Pathol
  doi: 10.1016/j.ajpath.2016.12.011
– volume: 74
  year: 1984
  ident: B8
  article-title: Structural-Functional Relationships in Diabetic Nephropathy
  publication-title: J Clin Invest
  doi: 10.1172/JCI111523
– volume: 17
  year: 2016
  ident: B49
  article-title: Role of mTOR Inhibitors in Kidney Disease
  publication-title: Int J Mol Sci
  doi: 10.3390/ijms17060975
– volume: 29
  year: 2018
  ident: B37
  article-title: Wnt9a Promotes Renal Fibrosis by Accelerating Cellular Senescence in Tubular Epithelial Cells
  publication-title: J Am Soc Nephrol
  doi: 10.1681/ASN.2017050574
– volume: 33
  start-page: 79
  year: 2015
  ident: B55
  article-title: Programmed Necrosis in the Cross Talk of Cell Death and Inflammation
  publication-title: Annu Rev Immunol
  doi: 10.1146/annurev-immunol-032414-112248
– volume: 7
  year: 2012
  ident: B83
  article-title: Autophagy Suppresses RIP Kinase-Dependent Necrosis Enabling Survival to mTOR Inhibition
  publication-title: PloS One
  doi: 10.1371/journal.pone.0041831
– volume: 29
  year: 2015
  ident: B54
  article-title: The Renoprotective Role of Autophagy Activation in Proximal Tubular Epithelial Cells in Diabetic Nephropathy
  publication-title: J Diabetes Complications
  doi: 10.1016/j.jdiacomp.2015.07.021
– volume: 21
  year: 2020
  ident: B6
  article-title: Emerging Connectivity of Programmed Cell Death Pathways and its Physiological Implications
  publication-title: Nat Rev Mol Cell Biol
  doi: 10.1038/s41580-020-0270-8
– volume: 15
  year: 2020
  ident: B60
  article-title: Angiotensin II Triggers RIPK3-MLKL-Mediated Necroptosis by Activating the Fas/FasL Signaling Pathway in Renal Tubular Cells
  publication-title: PloS One
  doi: 10.1371/journal.pone.0228385
– volume: 73
  year: 2016
  ident: B56
  article-title: Necroptosis-Independent Signaling by the RIP Kinases in Inflammation
  publication-title: Cell Mol Life Sci
  doi: 10.1007/s00018-016-2203-4
– volume: 7
  start-page: 427
  year: 2019
  ident: B50
  article-title: Research Digest: SGLT2 Inhibition in Kidney and Liver Disease-Science Direct
  publication-title: Lancet Diabetes Endocrinol
  doi: 10.1016/S2213-8587(19)30160-3
– volume: 49
  year: 2000
  ident: B64
  article-title: Early Glomerular Macrophage Recruitment in Streptozotocin-Induced Diabetic Rats
  publication-title: Diabetes
  doi: 10.2337/diabetes.49.3.466
– volume: 44
  year: 2012
  ident: B27
  article-title: Genome Stability, Progressive Kidney Failure and Aging
  publication-title: Nat Genet
  doi: 10.1038/ng.2363
– volume: 192
  start-page: 1
  year: 2002
  ident: B43
  article-title: Cellular Response to Oxidative Stress: Signaling for Suicide and Survival
  publication-title: J Cell Physiol
  doi: 10.1002/jcp.10119
– volume: 63
  year: 2004
  ident: B63
  article-title: Advanced Glycation End Products and Vascular Inflammation: Implications for Accelerated Atherosclerosis in Diabetes
  publication-title: Cardiovasc Res
  doi: 10.1016/j.cardiores.2004.05.001
– volume: 524
  year: 2015
  ident: B34
  article-title: Mechanism of Phospho-Ubiquitin-Induced PARKIN Activation
  publication-title: Nature
  doi: 10.1038/nature14879
– volume: 36
  year: 2015
  ident: B66
  article-title: Involvement of Endoplasmic Reticulum Stress in Angiotensin II-Induced NLRP3 Inflammasome Activation in Human Renal Proximal Tubular Cells
  publication-title: vitro. Acta Pharmacol Sin
  doi: 10.1038/aps.2015.21
– volume: 12
  year: 2021
  ident: B76
  article-title: Ferroptosis Enhanced Diabetic Renal Tubular Injury via HIF-1α/HO-1 Pathway in Db/Db Mice
  publication-title: Front Endocrinol
  doi: 10.3389/fendo.2021.626390
– volume: 26
  year: 2007
  ident: B78
  article-title: Functional and Physical Interaction Between Bcl-X (L) and BH3-Like Domain in Beclin-1
  publication-title: EMBO J
  doi: 10.1038/sj.emboj.7601689
– volume: 456
  start-page: 298
  year: 2015
  ident: B85
  article-title: RIPK3 Regulates P62-LC3 Complex Formation via the Caspase-8-Dependent Cleavage of P62
  publication-title: Biochem Biophys Res Commun
  doi: 10.1016/j.bbrc.2014.11.075
– volume: 513
  year: 2014
  ident: B89
  article-title: RIPK1 Ensures Intestinal Homeostasis by Protecting the Epithelium Against Apoptosis
  publication-title: Nature
  doi: 10.1038/nature13706
– volume: 267
  year: 2009
  ident: B24
  article-title: Telomere Length and Progression of Diabetic Nephropathy in Patients With Type 1 Diabetes
  publication-title: J Intern Med
  doi: 10.1111/j.1365-2796.2009.02139.x
– volume: 190
  year: 2013
  ident: B67
  article-title: Inflammasome-Independent NLRP3 Augments TGF-β Signaling in Kidney Epithelium
  publication-title: J Immunol
  doi: 10.4049/jimmunol.1201959
– volume: 3
  year: 2018
  ident: B62
  article-title: Renin-Angiotensin-Aldosterone System Activation in Long-Standing Type 1 Diabetes
  publication-title: JCI Insight
  doi: 10.1172/jci.insight.96968
– volume: 162
  year: 2021
  ident: B77
  article-title: Inhibition of Ferroptosis by Up-Regulating Nrf2 Delayed the Progression of Diabetic Nephropathy
  publication-title: Free Radic Biol Med
  doi: 10.1016/j.freeradbiomed.2020.10.323
– volume: 96
  year: 2016
  ident: B18
  article-title: Ergothioneine Oxidation in the Protection Against High-Glucose Induced Endothelial Senescence: Involvement of SIRT1 and SIRT6
  publication-title: Free Rad Biol Med
  doi: 10.1016/j.freeradbiomed.2016.04.013
– volume: 888
  year: 2020
  ident: B73
  article-title: Ferroptosis Involves in Renal Tubular Cell Death in Diabetic Nephropathy
  publication-title: Eur J Pharmacol
  doi: 10.1016/j.ejphar.2020.173574
– volume: 13
  year: 2012
  ident: B57
  article-title: Non-Apoptotic Functions of Apoptosis-Regulatory Proteins
  publication-title: EMBO Rep
  doi: 10.1038/embor.2012.19
– volume: 11
  year: 2006
  ident: B61
  article-title: Chronically Increased Intrarenal Angiotensin II Causes Nephropathy in an Animal Model of Type 2 Diabetes
  publication-title: Front Biosci
  doi: 10.2741/1853
– volume: 19
  year: 2013
  ident: B16
  article-title: Sirt1-Claudin-1 Crosstalk Regulates Renal Function
  publication-title: Nat Med
  doi: 10.1038/nm.3386
– volume: 343
  year: 2014
  ident: B91
  article-title: Activity of Protein Kinase RIPK3 Determines Whether Cells Die by Necroptosis or Apoptosis
  publication-title: Science
  doi: 10.1126/science.1249361
– volume: 91
  year: 2011
  ident: B38
  article-title: Inhibition of Inflammation by Pentosan Polysulfate Impedes the Development and Progression of Severe Diabetic Nephropathy in Aging C57B6 Mice
  publication-title: Lab Invest
  doi: 10.1038/labinvest.2011.93
– volume: 8
  year: 2007
  ident: B42
  article-title: The Apoptosome: Signalling Platform of Cell Death
  publication-title: Nat Rev Mol Cell Biol
  doi: 10.1038/nrm2153
– volume: 300
  year: 2011
  ident: B10
  article-title: The Proximal Tubule in the Pathophysiology of the Diabetic Kidney
  publication-title: Am J Physiol Regul Integr Comp Physiol
  doi: 10.1152/ajpregu.00809.2010
– volume: 1
  start-page: 15018
  year: 2015
  ident: B3
  article-title: Diabetic Kidney Disease
  publication-title: Nat Rev Dis Primers
  doi: 10.1038/nrdp.2015.18
– volume: 12
  start-page: 160
  year: 2021
  ident: B74
  article-title: Characterization of Ferroptosis in Kidney Tubular Cell Death Under Diabetic Conditions
  publication-title: Cell Death Dis
  doi: 10.1038/s41419-021-03452-x
– volume: 7
  year: 2012
  ident: B88
  article-title: CHOP Potentially Co-Operates With FOXO3a in Neuronal Cells to Regulate PUMA and BIM Expression in Response to ER Stress
  publication-title: PloS One
  doi: 10.1371/journal.pone.0039586
– volume: 23
  year: 2008
  ident: B14
  article-title: Prevalence of Atubular Glomeruli in Type 2 Diabetic Patients With Nephropathy
  publication-title: Nephrol Dial Transplant
  doi: 10.1093/ndt/gfn351
– volume: 10
  year: 2015
  ident: B41
  article-title: Protective Role of PGC-1α in Diabetic Nephropathy Is Associated With the Inhibition of ROS Through Mitochondrial Dynamic Remodeling
  publication-title: PloS One
  doi: 10.1371/journal.pone.0125176
– volume: 115
  year: 2005
  ident: B47
  article-title: Autophagy in Cell Death: An Innocent Convict
  publication-title: J Clin Invest
  doi: 10.1172/JCI26390
– volume: 12
  year: 2017
  ident: B1
  article-title: Diagnosis and Management of Type 2 Diabetic Kidney Disease
  publication-title: Clin J Am Soc Nephrol
  doi: 10.2215/CJN.11111016
– volume: 369
  start-page: 75
  year: 2017
  ident: B30
  article-title: Epigenetics of Kidney Disease
  publication-title: Cell Tissue Res
  doi: 10.1007/s00441-017-2588-x
– volume: 28
  year: 2014
  ident: B19
  article-title: Hyperglycemia Causes Cellular Senescence via a SGLT2 and P21-Dependent Pathway in Proximal Tubules in the Early Stage of Diabetic Nephropathy
  publication-title: J Diabetes Complications
  doi: 10.1016/j.jdiacomp.2014.05.010
– volume: 26
  year: 2015
  ident: B40
  article-title: Disruption of Renal Tubular Mitochondrial Quality Control by Myo-Inositol Oxygenase in Diabetic Kidney Disease
  publication-title: J Am Soc Nephrol
  doi: 10.1681/ASN.2014050457
– volume: 66
  start-page: 791
  year: 2017
  ident: B11
  article-title: Proximal Tubulopathy: Prime Mover and Key Therapeutic Target in Diabetic Kidney Disease
  publication-title: Diabetes
  doi: 10.2337/db16-0796
– volume: 12
  year: 2016
  ident: B87
  article-title: Autophagy Promotes Ferroptosis by Degradation of Ferritin
  publication-title: Autophagy
  doi: 10.1080/15548627.2016.1187366
– volume: 6
  year: 2017
  ident: B46
  article-title: Autophagic Cell Death is Dependent on Lysosomal Membrane Permeability Through Bax and Bak
  publication-title: eLife
  doi: 10.7554/eLife.30543
– volume: 133
  start-page: 153
  year: 2019
  ident: B72
  article-title: Iron Catalysis of Lipid Peroxidation in Ferroptosis: Regulated Enzymatic or Random Free Radical Reaction
  publication-title: Free Radic Biol Med
  doi: 10.1016/j.freeradbiomed.2018.09.008
– volume: 34
  year: 2021
  ident: B51
  article-title: Totally Tubular, Dude: Rethinking DKD Pathogenesis in the Wake of SGLT2i Data
  publication-title: J Nephrol
  doi: 10.1007/s40620-020-00868-0
– volume: 64
  year: 2015
  ident: B44
  article-title: ASK1 Inhibitor Halts Progression of Diabetic Nephropathy in Nos3-Deficient Mice
  publication-title: Diabetes
  doi: 10.2337/db15-0384
– volume: 17
  year: 2010
  ident: B79
  article-title: Apoptosis Blocks Beclin 1-Dependent Autophagosome Synthesis: An Effect Rescued by Bcl-Xl
  publication-title: Cell Death Differ
  doi: 10.1038/cdd.2009.121
– volume: 20
  year: 2009
  ident: B13
  article-title: Impaired Tubular Uptake Explains Albuminuria in Early Diabetic Nephropathy
  publication-title: J Am Soc Nephrol
  doi: 10.1681/ASN.2008050503
– volume: 124
  year: 2014
  ident: B31
  article-title: KLF4-Dependent Epigenetic Remodeling Modulates Podocyte Phenotypes and Attenuates Proteinuria
  publication-title: J Clin Invest
  doi: 10.1172/JCI69557
– volume: 194
  year: 2016
  ident: B58
  article-title: Necroptosis: A Novel Cell Death Modality and its Potential Relevance for Critical Care Medicine
  publication-title: Am J Respir Crit Care Med
  doi: 10.1164/rccm.201510-2106CI
– volume: 15
  year: 2014
  ident: B93
  article-title: RNA Viruses Promote Activation of the NLRP3 Inflammasome Through a RIP1-RIP3-DRP1 Signaling Pathway
  publication-title: Nat Immunol
  doi: 10.1038/ni.3015
– volume: 187
  year: 2011
  ident: B65
  article-title: Cutting Edge: Reactive Oxygen Species Inhibitors Block Priming, But Not Activation, of the NLRP3 Inflammasome
  publication-title: J Immunol
  doi: 10.4049/jimmunol.1100613
– volume: 23
  year: 2016
  ident: B26
  article-title: Oxidative Guanine Base Damage Regulates Human Telomerase Activity
  publication-title: Nat Struct Mol Biol
  doi: 10.1038/nsmb.3319
– volume: 12
  year: 2019
  ident: B70
  article-title: Curcumin and (-)- Epigallocatechin-3-Gallate Protect Murine MIN6 Pancreatic Beta-Cells Against Iron Toxicity and Erastin-Induced Ferroptosis
  publication-title: Pharmaceuticals
  doi: 10.3390/ph12010026
– volume: 49
  year: 2006
  ident: B23
  article-title: Chromosomal Telomere Attrition as a Mechanism for the Increased Risk of Epithelial Cancers and Senescent Phenotypes in Type 2 Diabetes
  publication-title: Diabetologia
  doi: 10.1007/s00125-006-0322-4
– volume: 3
  year: 2018
  ident: B52
  article-title: SGLT2 Inhibitor Dapagliflozin Limits Podocyte Damage in Proteinuric non-Diabetic Nephropathy
  publication-title: JCI Insight
  doi: 10.1172/jci.insight.98720
– volume: 311
  year: 2016
  ident: B9
  article-title: The Proximal Tubule is the Primary Target of Injury and Progression of Kidney Disease: Role of the Glomerulotubular Junction
  publication-title: Am J Physiol Renal Physiol
  doi: 10.1152/ajprenal.00164.2016
– volume: 19
  year: 2013
  ident: B15
  article-title: Renal Tubular Sirt1 Attenuates Diabetic Albuminuria by Epigenetically Suppressing Claudin-1 Overexpression in Podocytes
  publication-title: Nat Med
  doi: 10.1038/nm.3363
– volume: 339
  year: 1998
  ident: B2
  article-title: Pathophysiology of Progressive Nephropathies
  publication-title: N Engl J Med
  doi: 10.1056/NEJM199811123392007
– volume: 27
  year: 2020
  ident: B86
  article-title: Autophagy-Dependent Ferroptosis: Machinery and Regulation
  publication-title: Cell Chem Biol
  doi: 10.1016/j.chembiol.2020.02.005
– volume: 17
  year: 2020
  ident: B53
  article-title: SMAD3 Promotes Autophagy Dysregulation by Triggering Lysosome Depletion in Tubular Epithelial Cells in Diabetic Nephropathy
  publication-title: Autophagy
  doi: 10.1080/15548627.2020.1824694
– volume: 2019
  start-page: 1
  year: 2019
  ident: B4
  article-title: The Signaling of Cellular Senescence in Diabetic Nephropathy
  publication-title: Oxid Med Cell Longev
  doi: 10.1155/2019/7495629
– volume: 30
  year: 2015
  ident: B7
  article-title: New Developments Concerning the Proximal Tubule in Diabetic Nephropathy: In Vitro Models and Mechanisms
  publication-title: Nephrol Dialysis Transplant
  doi: 10.1093/ndt/gfv264
– volume: 30
  year: 2019
  ident: B12
  article-title: Diabetic Kidney Diseases Revisited: A New Perspective for a New Era
  publication-title: Mol Metab
  doi: 10.1016/j.molmet.2019.10.005
– volume: 9
  year: 2008
  ident: B45
  article-title: Autophagic Cell Death: The Story of a Misnomer
  publication-title: Nat Rev Mol Cell Biol
  doi: 10.1038/nrm2529
– volume: 6
  start-page: 6282
  year: 2015
  ident: B59
  article-title: RIPK3 Promotes Cell Death and NLRP3 Inflammasome Activation in the Absence of MLKL
  publication-title: Nat Commun
  doi: 10.1038/ncomms7282
– volume: 171
  year: 2017
  ident: B75
  article-title: Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease
  publication-title: Cell
  doi: 10.1016/j.cell.2017.09.021
– volume: 29
  year: 2019
  ident: B5
  article-title: The Molecular Machinery of Regulated Cell Death
  publication-title: Cell Res
  doi: 10.1038/s41422-019-0164-5
– volume: 23
  year: 2009
  ident: B28
  article-title: An Operational Definition of Epigenetics
  publication-title: Genes Dev
  doi: 10.1101/gad.1787609
– volume: 24
  year: 2010
  ident: B36
  article-title: Dietary and Genetic Evidence for Phosphate Toxicity Accelerating Mammalian Aging
  publication-title: FASEB J
  doi: 10.1096/fj.09-152488
– volume: 5
  year: 2014
  ident: B71
  article-title: Epidemiological Associations Between Iron and Cardiovascular Disease and Diabetes
  publication-title: Front Pharmacol
  doi: 10.3389/fphar.2014.00117
– volume: 1
  year: 2010
  ident: B80
  article-title: Caspase-Mediated Cleavage of Beclin-1 Inactivates Beclin-1-Induced Autophagy and Enhances Apoptosis by Promoting the Release of Proapoptotic Factors From Mitochondria
  publication-title: Cell Death Dis
  doi: 10.1038/cddis.2009.16
SSID ssj0000401998
Score 2.5033424
SecondaryResourceType review_article
Snippet Cellular senescence is frequently evident at etiologic sites of chronic diseases and involves essentially irreversible arrest of cell proliferation, increased...
SourceID doaj
pubmedcentral
proquest
crossref
SourceType Open Website
Open Access Repository
Aggregation Database
Enrichment Source
Index Database
StartPage 924299
SubjectTerms cellular senescence
diabetic kidney disease (DKD)
diabetic tubulopathy
Endocrinology
regulated cell death
regulated cell death (RCD)
SummonAdditionalLinks – databaseName: Scholars Portal Journals: Open Access
  dbid: M48
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV3daxQxEA-1gvgifuJZlQg-CVtzm02yeRDR2lKU80F70LeQz3qw5Op9QPvfO5PdKy4Un3xZ9mPCJjOZzG9IZoaQt6113sWoqqBiUzUiNZWbSlkJYTWzbupahbHDs-_ydN58PRfne2RX3mpg4PpW1w7rSc1X3eHV7-uPoPAf0OMEe_s-xRwwjq-uD8GbgPX1DrkLhkmhns4GtF8WZvAlwLvo9zZvbzmyTiWJ_wh5js9N_mWITh6SBwOCpJ96kT8iezE_Jvdmwx75E-KPYtfh4VL6E9cxj6pLbQ70R192PgaKFPQLgj-6TPRs6wr58SXGZ3QwIQvBmi4y7Q_MLDz9tgg5XsNz2c95SuYnx2dHp9VQSqHygMA2lebgCXoW_DR4q7hTdSOsAHDAnJuypKJT3lnHW8-Yg0sSkcVGcqeZF3WI_BnZz8scnxMaOQa_psC4Dk20Gu7xWdbJO8BiaULYjoXGD3nGsdxFZ8DfQK6bwnWDXDc91yfk3U2Tyz7Jxr-IP6NcbggxP3Z5sVxdmEHdjGptrUMrWhUk9DU5CaYapp5KXvOg7YS82UnVgD7hJonNcbldGxhcyVjUyAlRI3GP_jj-khe_SmZuDWBQcfnif3TxgNzHUeOxtLp9SfY3q218BQBo416Xaf0HJdMIBw
  priority: 102
  providerName: Scholars Portal
Title Cellular Senescence and Regulated Cell Death of Tubular Epithelial Cells in Diabetic Kidney Disease
URI https://www.proquest.com/docview/2691047846
https://pubmed.ncbi.nlm.nih.gov/PMC9273736
https://doaj.org/article/78a29d8587d64fdfb6303ab17fc93d9a
Volume 13
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQD4gLKo-KLQ8ZiRNSWid-xcdSWirQcoBW2pvlp1hp5a3a3QP_vjNOWjYXuHCx4mSS2OOx_Y3mYUI-9M4Hn5Juok6iETKLxrdKNVI6w5xvfa8xdnj-XV1cia8Ludg56gt9wob0wAPjjnXvOhN72euoRI7ZK1h04SM6B8OjqdAI9rwdZaquwaA2gCIxmDFBCzPHOZWIwX5ddwQqR1dzvf7ZiGq-_gnInLpI7uw55_vk6QgW6cnQyGfkUSrPyeP5aA5_QcJpWq3Qj5T-xCUr4CylrkT6YzhhPkWKFPQz4jy6zvRy6yv52TWGYqxA9irBLV0WOvjGLAP9towl_YZ6Nd28JFfnZ5enF814akITAGxtGsNB6QsshjYGp7nXnZBOAg5g3rcs6-R18M7zPjDmocgysSQU94YF2cXED8heWZf0itDEMc41R8ZNFMkZuMa66nLwALvyjLB7FtowphTHky1WFlQL5LqtXLfIdTtwfUY-PrxyPeTT-BvxJxyXB0JMhV1vgIDYUUDsvwRkRt7fj6qFqYP2EFfSentroXM1OZFQM6Inwz354_RJWf6qSbgN4D7N1eH_aOJr8gR7jR5oXf-G7G1utuktYJ2Nf1fFGsovixbKuejvADMFAcU
linkProvider Directory of Open Access Journals
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=Cellular+Senescence+and+Regulated+Cell+Death+of+Tubular+Epithelial+Cells+in+Diabetic+Kidney+Disease&rft.jtitle=Frontiers+in+endocrinology+%28Lausanne%29&rft.au=Shuang+Shen&rft.au=Chuanyuan+Ji&rft.au=Kaifeng+Wei&rft.date=2022-06-28&rft.pub=Frontiers+Media+S.A&rft.eissn=1664-2392&rft.volume=13&rft_id=info:doi/10.3389%2Ffendo.2022.924299&rft.externalDBID=DOA&rft.externalDocID=oai_doaj_org_article_78a29d8587d64fdfb6303ab17fc93d9a
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1664-2392&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1664-2392&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1664-2392&client=summon