Long‐term intake of phenolic compounds attenuates age‐related cardiac remodeling

With the onset of advanced age, cardiac‐associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence, fibroblast proliferation, inflammation, and hypertrophy. The imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes...

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Published inAging cell Vol. 18; no. 2; pp. e12894 - n/a
Main Authors Chacar, Stéphanie, Hajal, Joelle, Saliba, Youakim, Bois, Patrick, Louka, Nicolas, Maroun, Richard G., Faivre, Jean‐François, Fares, Nassim
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.04.2019
Wiley Open Access
John Wiley and Sons Inc
Subjects
Administration, Oral
Age
Aging
Analysis
Animals
Antioxidants
Apoptosis
Apoptosis - drug effects
Ca2+/calmodulin-dependent protein kinase II
Calcineurin
Calcium-binding protein
Calmodulin
cardiac remodeling
Cardiology and cardiovascular system
Cardiomyocytes
Diet
DNA damage
Dose-Response Relationship, Drug
Echocardiography
Enzymes
Extracellular matrix
Extracellular signal-regulated kinase
Fibrosis
Glycogen
Glycogen synthase kinase 3
Heart
Heart enlargement
Human health and pathology
Hypertrophy
Inflammation
Kinases
Life Sciences
Male
Models, Biological
NF-AT protein
Original
Oxidative Stress
Oxidative Stress - drug effects
Phenolic compounds
Phenols
Phenols - administration & dosage
Phenols - pharmacology
Preservation
Rats
Rats, Wistar
Reactive Oxygen Species
Reactive Oxygen Species - metabolism
Ribonucleic acid
RNA
Senescence
Smad protein
Synthesis
T cells
Transcription factors
Transforming growth factors
Ventricle
Ventricular Dysfunction, Left
Ventricular Dysfunction, Left - metabolism
Ventricular Dysfunction, Left - prevention & control
Ventricular Remodeling
Ventricular Remodeling - drug effects
phenolic compounds
fibrosis
aging
hypertrophy
oxidative stress
cardiac remodeling
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Abstract With the onset of advanced age, cardiac‐associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence, fibroblast proliferation, inflammation, and hypertrophy. The imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes is greatly enhanced in aging cells, promoting cardiac remodeling. In this work, we studied the long‐term impact of phenolic compounds (PC) on age‐associated cardiac remodeling. Three‐month‐old Wistar rats were treated for 14 months till middle‐age with either 2.5, 5, 10, or 20 mg kg−1 day−1 of PC. PC treatment showed a dose‐dependent preservation of cardiac ejection fraction and fractional shortening as well as decreased hypertrophy reflected by left ventricular chamber diameter and posterior wall thickness as compared to untreated middle‐aged control animals. Analyses of proteins from cardiac tissue showed that PC attenuated several hypertrophic pathways including calcineurin/nuclear factor of activated T cells (NFATc3), calcium/calmodulin‐dependent kinase II (CAMKII), extracellular regulated kinase 1/2 (ERK1/2), and glycogen synthase kinase 3ß (GSK 3ß). PC‐treated groups exhibited reduced plasma inflammatory and fibrotic markers and revealed as well ameliorated extracellular matrix remodeling and interstitial inflammation by a downregulated p38 pathway. Myocardia from PC‐treated middle‐aged rats presented less fibrosis with suppression of profibrotic transforming growth factor‐ß1 (TGF‐ß1) Smad pathway. Additionally, reduction of apoptosis and oxidative damage in the PC‐treated groups was reflected by elevated antioxidant enzymes and reduced RNA/DNA damage markers. Our findings pinpoint that a daily consumption of phenolic compounds could preserve the heart from the detrimental effects of aging storm.
AbstractList With the onset of advanced age, cardiac-associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence, fibroblast proliferation, inflammation, and hypertrophy. The imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes is greatly enhanced in aging cells, promoting cardiac remodeling. In this work, we studied the long-term impact of phenolic compounds (PC) on age-associated cardiac remodeling. Three-month-old Wistar rats were treated for 14 months till middle-age with either 2.5, 5, 10, or 20 mg kg[sup.−1] day[sup.−1] of PC. PC treatment showed a dose-dependent preservation of cardiac ejection fraction and fractional shortening as well as decreased hypertrophy reflected by left ventricular chamber diameter and posterior wall thickness as compared to untreated middle-aged control animals. Analyses of proteins from cardiac tissue showed that PC attenuated several hypertrophic pathways including calcineurin/nuclear factor of activated T cells (NFATc3), calcium/calmodulin-dependent kinase II (CAMKII), extracellular regulated kinase 1/2 (ERK1/2), and glycogen synthase kinase 3ß (GSK 3ß). PC-treated groups exhibited reduced plasma inflammatory and fibrotic markers and revealed as well ameliorated extracellular matrix remodeling and interstitial inflammation by a downregulated p38 pathway. Myocardia from PC-treated middle-aged rats presented less fibrosis with suppression of profibrotic transforming growth factor-ß1 (TGF-ß1) Smad pathway. Additionally, reduction of apoptosis and oxidative damage in the PC-treated groups was reflected by elevated antioxidant enzymes and reduced RNA/DNA damage markers. Our findings pinpoint that a daily consumption of phenolic compounds could preserve the heart from the detrimental effects of aging storm.
With the onset of advanced age, cardiac‐associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence, fibroblast proliferation, inflammation, and hypertrophy. The imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes is greatly enhanced in aging cells, promoting cardiac remodeling. In this work, we studied the long‐term impact of phenolic compounds (PC) on age‐associated cardiac remodeling. Three‐month‐old Wistar rats were treated for 14 months till middle‐age with either 2.5, 5, 10, or 20 mg kg−1 day−1 of PC. PC treatment showed a dose‐dependent preservation of cardiac ejection fraction and fractional shortening as well as decreased hypertrophy reflected by left ventricular chamber diameter and posterior wall thickness as compared to untreated middle‐aged control animals. Analyses of proteins from cardiac tissue showed that PC attenuated several hypertrophic pathways including calcineurin/nuclear factor of activated T cells (NFATc3), calcium/calmodulin‐dependent kinase II (CAMKII), extracellular regulated kinase 1/2 (ERK1/2), and glycogen synthase kinase 3ß (GSK 3ß). PC‐treated groups exhibited reduced plasma inflammatory and fibrotic markers and revealed as well ameliorated extracellular matrix remodeling and interstitial inflammation by a downregulated p38 pathway. Myocardia from PC‐treated middle‐aged rats presented less fibrosis with suppression of profibrotic transforming growth factor‐ß1 (TGF‐ß1) Smad pathway. Additionally, reduction of apoptosis and oxidative damage in the PC‐treated groups was reflected by elevated antioxidant enzymes and reduced RNA/DNA damage markers. Our findings pinpoint that a daily consumption of phenolic compounds could preserve the heart from the detrimental effects of aging storm.
With the onset of advanced age, cardiac‐associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence, fibroblast proliferation, inflammation, and hypertrophy. The imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes is greatly enhanced in aging cells, promoting cardiac remodeling. In this work, we studied the long‐term impact of phenolic compounds (PC) on age‐associated cardiac remodeling. Three‐month‐old Wistar rats were treated for 14 months till middle‐age with either 2.5, 5, 10, or 20 mg kg−1 day−1 of PC. PC treatment showed a dose‐dependent preservation of cardiac ejection fraction and fractional shortening as well as decreased hypertrophy reflected by left ventricular chamber diameter and posterior wall thickness as compared to untreated middle‐aged control animals. Analyses of proteins from cardiac tissue showed that PC attenuated several hypertrophic pathways including calcineurin/nuclear factor of activated T cells (NFATc3), calcium/calmodulin‐dependent kinase II (CAMKII), extracellular regulated kinase 1/2 (ERK1/2), and glycogen synthase kinase 3ß (GSK 3ß). PC‐treated groups exhibited reduced plasma inflammatory and fibrotic markers and revealed as well ameliorated extracellular matrix remodeling and interstitial inflammation by a downregulated p38 pathway. Myocardia from PC‐treated middle‐aged rats presented less fibrosis with suppression of profibrotic transforming growth factor‐ß1 (TGF‐ß1) Smad pathway. Additionally, reduction of apoptosis and oxidative damage in the PC‐treated groups was reflected by elevated antioxidant enzymes and reduced RNA/DNA damage markers. Our findings pinpoint that a daily consumption of phenolic compounds could preserve the heart from the detrimental effects of aging storm.
With the onset of advanced age, cardiac-associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence, fibroblast proliferation, inflammation, and hypertrophy. The imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes is greatly enhanced in aging cells, promoting cardiac remodeling. In this work, we studied the long-term impact of phenolic compounds (PC) on age-associated cardiac remodeling. Three-month-old Wistar rats were treated for 14 months till middle-age with either 2.5, 5, 10, or 20 mg kg-1 day-1 of PC. PC treatment showed a dose-dependent preservation of cardiac ejection fraction and fractional shortening as well as decreased hypertrophy reflected by left ventricular chamber diameter and posterior wall thickness as compared to untreated middle-aged control animals. Analyses of proteins from cardiac tissue showed that PC attenuated several hypertrophic pathways including calcineurin/nuclear factor of activated T cells (NFATc3), calcium/calmodulin-dependent kinase II (CAMKII), extracellular regulated kinase 1/2 (ERK1/2), and glycogen synthase kinase 3ß (GSK 3ß). PC-treated groups exhibited reduced plasma inflammatory and fibrotic markers and revealed as well ameliorated extracellular matrix remodeling and interstitial inflammation by a downregulated p38 pathway. Myocardia from PC-treated middle-aged rats presented less fibrosis with suppression of profibrotic transforming growth factor-ß1 (TGF-ß1) Smad pathway. Additionally, reduction of apoptosis and oxidative damage in the PC-treated groups was reflected by elevated antioxidant enzymes and reduced RNA/DNA damage markers. Our findings pinpoint that a daily consumption of phenolic compounds could preserve the heart from the detrimental effects of aging storm.With the onset of advanced age, cardiac-associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence, fibroblast proliferation, inflammation, and hypertrophy. The imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes is greatly enhanced in aging cells, promoting cardiac remodeling. In this work, we studied the long-term impact of phenolic compounds (PC) on age-associated cardiac remodeling. Three-month-old Wistar rats were treated for 14 months till middle-age with either 2.5, 5, 10, or 20 mg kg-1 day-1 of PC. PC treatment showed a dose-dependent preservation of cardiac ejection fraction and fractional shortening as well as decreased hypertrophy reflected by left ventricular chamber diameter and posterior wall thickness as compared to untreated middle-aged control animals. Analyses of proteins from cardiac tissue showed that PC attenuated several hypertrophic pathways including calcineurin/nuclear factor of activated T cells (NFATc3), calcium/calmodulin-dependent kinase II (CAMKII), extracellular regulated kinase 1/2 (ERK1/2), and glycogen synthase kinase 3ß (GSK 3ß). PC-treated groups exhibited reduced plasma inflammatory and fibrotic markers and revealed as well ameliorated extracellular matrix remodeling and interstitial inflammation by a downregulated p38 pathway. Myocardia from PC-treated middle-aged rats presented less fibrosis with suppression of profibrotic transforming growth factor-ß1 (TGF-ß1) Smad pathway. Additionally, reduction of apoptosis and oxidative damage in the PC-treated groups was reflected by elevated antioxidant enzymes and reduced RNA/DNA damage markers. Our findings pinpoint that a daily consumption of phenolic compounds could preserve the heart from the detrimental effects of aging storm.
With the onset of advanced age, cardiac-associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence, fibroblast proliferation, inflammation, and hypertrophy. The imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes is greatly enhanced in aging cells, promoting cardiac remodeling. In this work, we studied the long-term impact of phenolic compounds (PC) on age-associated cardiac remodeling. Three-month-old Wistar rats were treated for 14 months till middle-age with either 2.5, 5, 10, or 20 mg kg-1 day-1 of PC. PC treatment showed a dose-dependent preservation of cardiac ejection fraction and fractional shortening as well as decreased hypertrophy reflected by left ventricular chamber diameter and posterior wall thickness as compared to untreated middle-aged control animals. Analyses of proteins from cardiac tissue showed that PC attenuated several hypertrophic pathways including calcineurin/nuclear factor of activated T cells (NFATc3), calcium/calmodulin-dependent kinase II (CAMKII), extracellular regulated kinase 1/2 (ERK1/2), and glycogen synthase kinase 3ß (GSK 3ß). PC-treated groups exhibited reduced plasma inflammatory and fibrotic markers and revealed as well ameliorated extracellular matrix remodeling and interstitial inflammation by a downregulated p38 pathway. Myocardia from PC-treated middle-aged rats presented less fibrosis with suppression of profibrotic transforming growth factor-ß1 (TGF-ß1) Smad pathway. Additionally, reduction of apoptosis and oxidative damage in the PC-treated groups was reflected by elevated antioxidant enzymes and reduced RNA/DNA damage markers. Our findings pinpoint that a daily consumption of phenolic compounds could preserve the heart from the detrimental effects of aging storm.
With the onset of advanced age, cardiac-associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence, fibroblast proliferation, inflammation, and hypertrophy. The imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes is greatly enhanced in aging cells, promoting cardiac remodeling. In this work, we studied the long-term impact of phenolic compounds (PC) on age-associated cardiac remodeling. Three-month-old Wistar rats were treated for 14 months till middle-age with either 2.5, 5, 10, or 20 mg kg  day of PC. PC treatment showed a dose-dependent preservation of cardiac ejection fraction and fractional shortening as well as decreased hypertrophy reflected by left ventricular chamber diameter and posterior wall thickness as compared to untreated middle-aged control animals. Analyses of proteins from cardiac tissue showed that PC attenuated several hypertrophic pathways including calcineurin/nuclear factor of activated T cells (NFATc3), calcium/calmodulin-dependent kinase II (CAMKII), extracellular regulated kinase 1/2 (ERK1/2), and glycogen synthase kinase 3ß (GSK 3ß). PC-treated groups exhibited reduced plasma inflammatory and fibrotic markers and revealed as well ameliorated extracellular matrix remodeling and interstitial inflammation by a downregulated p38 pathway. Myocardia from PC-treated middle-aged rats presented less fibrosis with suppression of profibrotic transforming growth factor-ß1 (TGF-ß1) Smad pathway. Additionally, reduction of apoptosis and oxidative damage in the PC-treated groups was reflected by elevated antioxidant enzymes and reduced RNA/DNA damage markers. Our findings pinpoint that a daily consumption of phenolic compounds could preserve the heart from the detrimental effects of aging storm.
With the onset of advanced age, cardiac‐associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence, fibroblast proliferation, inflammation, and hypertrophy. The imbalance between levels of reactive oxygen species (ROS) and antioxidant enzymes is greatly enhanced in aging cells, promoting cardiac remodeling. In this work, we studied the long‐term impact of phenolic compounds (PC) on age‐associated cardiac remodeling. Three‐month‐old Wistar rats were treated for 14 months till middle‐age with either 2.5, 5, 10, or 20 mg kg −1  day −1 of PC. PC treatment showed a dose‐dependent preservation of cardiac ejection fraction and fractional shortening as well as decreased hypertrophy reflected by left ventricular chamber diameter and posterior wall thickness as compared to untreated middle‐aged control animals. Analyses of proteins from cardiac tissue showed that PC attenuated several hypertrophic pathways including calcineurin/nuclear factor of activated T cells (NFATc3), calcium/calmodulin‐dependent kinase II (CAMKII), extracellular regulated kinase 1/2 (ERK1/2), and glycogen synthase kinase 3ß (GSK 3ß). PC‐treated groups exhibited reduced plasma inflammatory and fibrotic markers and revealed as well ameliorated extracellular matrix remodeling and interstitial inflammation by a downregulated p38 pathway. Myocardia from PC‐treated middle‐aged rats presented less fibrosis with suppression of profibrotic transforming growth factor‐ß1 (TGF‐ß1) Smad pathway. Additionally, reduction of apoptosis and oxidative damage in the PC‐treated groups was reflected by elevated antioxidant enzymes and reduced RNA/DNA damage markers. Our findings pinpoint that a daily consumption of phenolic compounds could preserve the heart from the detrimental effects of aging storm.
Audience Academic
Author Saliba, Youakim
Maroun, Richard G.
Fares, Nassim
Bois, Patrick
Faivre, Jean‐François
Chacar, Stéphanie
Hajal, Joelle
Louka, Nicolas
AuthorAffiliation 3 Laboratoire Signalisation et Transports Ioniques Membranaires (STIM) Université de Poitiers Poitiers France
1 Faculté de Médecine, Laboratoire de Recherche en Physiologie et Physiopathologie, LRPP, Pôle Technologie Santé Université Saint Joseph Beyrouth Liban
2 Faculté des Sciences, Centre d’Analyses et de Recherche, UR GPF, Laboratoire CTA Université Saint‐Joseph Beyrouth Liban
AuthorAffiliation_xml – name: 2 Faculté des Sciences, Centre d’Analyses et de Recherche, UR GPF, Laboratoire CTA Université Saint‐Joseph Beyrouth Liban
– name: 1 Faculté de Médecine, Laboratoire de Recherche en Physiologie et Physiopathologie, LRPP, Pôle Technologie Santé Université Saint Joseph Beyrouth Liban
– name: 3 Laboratoire Signalisation et Transports Ioniques Membranaires (STIM) Université de Poitiers Poitiers France
Author_xml – sequence: 1
  givenname: Stéphanie
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  organization: Université de Poitiers
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  organization: Université Saint Joseph
– sequence: 3
  givenname: Youakim
  surname: Saliba
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  organization: Université Saint Joseph
– sequence: 4
  givenname: Patrick
  surname: Bois
  fullname: Bois, Patrick
  organization: Université de Poitiers
– sequence: 5
  givenname: Nicolas
  surname: Louka
  fullname: Louka, Nicolas
  organization: Université Saint‐Joseph
– sequence: 6
  givenname: Richard G.
  surname: Maroun
  fullname: Maroun, Richard G.
  organization: Université Saint‐Joseph
– sequence: 7
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– sequence: 8
  givenname: Nassim
  orcidid: 0000-0002-2935-2611
  surname: Fares
  fullname: Fares, Nassim
  email: nassim.fares@usj.edu.lb
  organization: Université Saint Joseph
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30680911$$D View this record in MEDLINE/PubMed
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Copyright 2018 The Authors. published by the Anatomical Society and John Wiley & Sons Ltd.
2018 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
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– notice: COPYRIGHT 2019 John Wiley & Sons, Inc.
– notice: 2019. 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: Distributed under a Creative Commons Attribution 4.0 International License
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Issue 2
Keywords phenolic compounds
fibrosis
aging
hypertrophy
oxidative stress
cardiac remodeling
Language English
License Attribution
2018 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0
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.
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Notes ObjectType-Article-1
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content type line 23
PMCID: PMC6413651
These authors contributed equally to this work, respectively.
ORCID 0000-0002-2935-2611
0000-0002-8153-0171
0000-0002-8995-9052
0000-0001-5645-5926
OpenAccessLink https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6413651/
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PublicationTitle Aging cell
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John Wiley and Sons Inc
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2015; 6
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Snippet With the onset of advanced age, cardiac‐associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence,...
With the onset of advanced age, cardiac-associated pathologies have increased in prevalence. The hallmarks of cardiac aging include cardiomyocyte senescence,...
SourceID pubmedcentral
hal
proquest
gale
crossref
pubmed
wiley
SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage e12894
SubjectTerms Administration, Oral
Age
Aging
Analysis
Animals
Antioxidants
Apoptosis
Apoptosis - drug effects
Ca2+/calmodulin-dependent protein kinase II
Calcineurin
Calcium-binding protein
Calmodulin
cardiac remodeling
Cardiology and cardiovascular system
Cardiomyocytes
Diet
DNA damage
Dose-Response Relationship, Drug
Echocardiography
Enzymes
Extracellular matrix
Extracellular signal-regulated kinase
Fibrosis
Glycogen
Glycogen synthase kinase 3
Heart
Heart enlargement
Human health and pathology
Hypertrophy
Inflammation
Kinases
Life Sciences
Male
Models, Biological
NF-AT protein
Original
Oxidative Stress
Oxidative Stress - drug effects
Phenolic compounds
Phenols
Phenols - administration & dosage
Phenols - pharmacology
Preservation
Rats
Rats, Wistar
Reactive Oxygen Species
Reactive Oxygen Species - metabolism
Ribonucleic acid
RNA
Senescence
Smad protein
Synthesis
T cells
Transcription factors
Transforming growth factors
Ventricle
Ventricular Dysfunction, Left
Ventricular Dysfunction, Left - metabolism
Ventricular Dysfunction, Left - prevention & control
Ventricular Remodeling
Ventricular Remodeling - drug effects
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Title Long‐term intake of phenolic compounds attenuates age‐related cardiac remodeling
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Facel.12894
https://www.ncbi.nlm.nih.gov/pubmed/30680911
https://www.proquest.com/docview/2190073334
https://www.proquest.com/docview/2179453069
https://hal.science/hal-02457531
https://pubmed.ncbi.nlm.nih.gov/PMC6413651
Volume 18
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