Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice
Male
Aging
Heart Diseases
QH301-705.5
Science
aging
Q
R
Mitochondria
mitochondria
Mice, Inbred C57BL
Mice
Oxidative Stress
oxidative stress
Medicine
Animals
diastolic dysfunction
Female
cardiac function
Biology (General)
Human Biology and Medicine
Energy Metabolism
Oligopeptides
Oxidation-Reduction
DOI:
10.7554/elife.55513
Publication Date:
2020-07-10T12:00:22Z
AUTHORS (22)
ABSTRACT
Diastolic dysfunction is a prominent feature of cardiac aging in both mice and humans. We show here that 8-week treatment old with the mitochondrial targeted peptide SS-31 (elamipretide) can substantially reverse this deficit. normalized increase proton leak reduced ROS cardiomyocytes from mice, accompanied by protein oxidation shift towards more thiol redox state hearts. Improved diastolic function was concordant increased phosphorylation cMyBP-C Ser282 but independent titin isoform shift. Late-life viral expression mitochondrial-targeted catalase (mCAT) produced similar functional benefits did not improve mCAT implicating normalizing oxidative stress as an overlapping mechanism. These results demonstrate pre-existing phenotypes be reversed targeting implicate energetics signaling therapeutic targets for aging.
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