Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice

Diastolic dysfunction is a prominent feature of cardiac aging in both mice and humans. We show here that 8-week treatment of old mice with the mitochondrial targeted peptide SS-31 (elamipretide) can substantially reverse this deficit. SS-31 normalized the increase in proton leak and reduced mitochon...

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Vydáno v:	eLife Ročník 9
Hlavní autoři:	Chiao, Ying Ann, Zhang, Huiliang, Sweetwyne, Mariya, Whitson, Jeremy, Ting, Ying Sonia, Basisty, Nathan, Pino, Lindsay K, Quarles, Ellen, Nguyen, Ngoc-Han, Campbell, Matthew D, Zhang, Tong, Gaffrey, Matthew J, Merrihew, Gennifer, Wang, Lu, Yue, Yongping, Duan, Dongsheng, Granzier, Henk L, Szeto, Hazel H, Qian, Wei-Jun, Marcinek, David, MacCoss, Michael J, Rabinovitch, Peter
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	England eLife Sciences Publications Ltd 10.07.2020 eLife Sciences Publications, Ltd
Témata:	Age Aging Aging - drug effects Animals BASIC BIOLOGICAL SCIENCES Cardiac function Cardiomyocytes Catalase Connectin diastolic dysfunction Energy Metabolism Female Fitness equipment Heart Diseases - drug therapy Heart Diseases - physiopathology Human Biology and Medicine Male Mice Mice, Inbred C57BL Mitochondria Mitochondria - physiology Mitochondrial DNA Oligopeptides - administration & dosage Oxidation-Reduction Oxidative Stress Phenotypes Phosphorylation Redox properties Rodents Running human biology mouse mitochondria diastolic dysfunction cardiac function medicine aging oxidative stress
ISSN:	2050-084X, 2050-084X
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Abstract	Diastolic dysfunction is a prominent feature of cardiac aging in both mice and humans. We show here that 8-week treatment of old mice with the mitochondrial targeted peptide SS-31 (elamipretide) can substantially reverse this deficit. SS-31 normalized the increase in proton leak and reduced mitochondrial ROS in cardiomyocytes from old mice, accompanied by reduced protein oxidation and a shift towards a more reduced protein thiol redox state in old hearts. Improved diastolic function was concordant with increased phosphorylation of cMyBP-C Ser282 but was independent of titin isoform shift. Late-life viral expression of mitochondrial-targeted catalase (mCAT) produced similar functional benefits in old mice and SS-31 did not improve cardiac function of old mCAT mice, implicating normalizing mitochondrial oxidative stress as an overlapping mechanism. These results demonstrate that pre-existing cardiac aging phenotypes can be reversed by targeting mitochondrial dysfunction and implicate mitochondrial energetics and redox signaling as therapeutic targets for cardiac aging.
AbstractList	Diastolic dysfunction is a prominent feature of cardiac aging in both mice and humans. We show here that 8-week treatment of old mice with the mitochondrial targeted peptide SS-31 (elamipretide) can substantially reverse this deficit. SS-31 normalized the increase in proton leak and reduced mitochondrial ROS in cardiomyocytes from old mice, accompanied by reduced protein oxidation and a shift towards a more reduced protein thiol redox state in old hearts. Improved diastolic function was concordant with increased phosphorylation of cMyBP-C Ser282 but was independent of titin isoform shift. Late-life viral expression of mitochondrial-targeted catalase (mCAT) produced similar functional benefits in old mice and SS-31 did not improve cardiac function of old mCAT mice, implicating normalizing mitochondrial oxidative stress as an overlapping mechanism. These results demonstrate that pre-existing cardiac aging phenotypes can be reversed by targeting mitochondrial dysfunction and implicate mitochondrial energetics and redox signaling as therapeutic targets for cardiac aging. Diastolic dysfunction is a prominent feature of cardiac aging in both mice and humans. We show here that 8-week treatment of old mice with the mitochondrial targeted peptide SS-31 (elamipretide) can substantially reverse this deficit. SS-31 normalized the increase in proton leak and reduced mitochondrial ROS in cardiomyocytes from old mice, accompanied by reduced protein oxidation and a shift towards a more reduced protein thiol redox state in old hearts. Improved diastolic function was concordant with increased phosphorylation of cMyBP-C Ser282 but was independent of titin isoform shift. Late-life viral expression of mitochondrial-targeted catalase (mCAT) produced similar functional benefits in old mice and SS-31 did not improve cardiac function of old mCAT mice, implicating normalizing mitochondrial oxidative stress as an overlapping mechanism. These results demonstrate that pre-existing cardiac aging phenotypes can be reversed by targeting mitochondrial dysfunction and implicate mitochondrial energetics and redox signaling as therapeutic targets for cardiac aging.Diastolic dysfunction is a prominent feature of cardiac aging in both mice and humans. We show here that 8-week treatment of old mice with the mitochondrial targeted peptide SS-31 (elamipretide) can substantially reverse this deficit. SS-31 normalized the increase in proton leak and reduced mitochondrial ROS in cardiomyocytes from old mice, accompanied by reduced protein oxidation and a shift towards a more reduced protein thiol redox state in old hearts. Improved diastolic function was concordant with increased phosphorylation of cMyBP-C Ser282 but was independent of titin isoform shift. Late-life viral expression of mitochondrial-targeted catalase (mCAT) produced similar functional benefits in old mice and SS-31 did not improve cardiac function of old mCAT mice, implicating normalizing mitochondrial oxidative stress as an overlapping mechanism. These results demonstrate that pre-existing cardiac aging phenotypes can be reversed by targeting mitochondrial dysfunction and implicate mitochondrial energetics and redox signaling as therapeutic targets for cardiac aging.
Author	Chiao, Ying Ann Zhang, Huiliang Sweetwyne, Mariya Ting, Ying Sonia Yue, Yongping Granzier, Henk L Gaffrey, Matthew J Whitson, Jeremy Pino, Lindsay K Quarles, Ellen Duan, Dongsheng Nguyen, Ngoc-Han Merrihew, Gennifer Wang, Lu Marcinek, David Basisty, Nathan Zhang, Tong Rabinovitch, Peter Szeto, Hazel H Qian, Wei-Jun MacCoss, Michael J Campbell, Matthew D
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Snippet	Diastolic dysfunction is a prominent feature of cardiac aging in both mice and humans. We show here that 8-week treatment of old mice with the mitochondrial...
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SubjectTerms	Age Aging Aging - drug effects Animals BASIC BIOLOGICAL SCIENCES Cardiac function Cardiomyocytes Catalase Connectin diastolic dysfunction Energy Metabolism Female Fitness equipment Heart Diseases - drug therapy Heart Diseases - physiopathology Human Biology and Medicine Male Mice Mice, Inbred C57BL Mitochondria Mitochondria - physiology Mitochondrial DNA Oligopeptides - administration & dosage Oxidation-Reduction Oxidative Stress Phenotypes Phosphorylation Redox properties Rodents Running
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Title	Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice
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