Abstract
We analyzed the effects of aging on protein abundance and acetylation, as well as the ability of the mitochondrial-targeted drugs elamipretide (SS-31) and nicotinamide mononucleotide (NMN) to reverse aging-associated changes in mouse hearts. Both drugs had a modest effect on restoring the abundance and acetylation of proteins that are altered with age, while also inducing additional changes. Age-related increases in protein acetylation were predominantly in mitochondrial pathways such as mitochondrial dysfunction, oxidative phosphorylation, and TCA cycle signaling. We further assessed how these age-related changes associated with diastolic function (Ea/Aa) and systolic function (fractional shortening under higher workload) measurements from echocardiography. These results identify a subset of protein abundance and acetylation changes in muscle, mitochondrial, and structural proteins that appear to be essential in regulating diastolic function in old hearts.
Original language | English |
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Pages (from-to) | 1621-1639 |
Number of pages | 19 |
Journal | GeroScience |
Volume | 44 |
Issue number | 3 |
DOIs | |
State | Published - Jun 2022 |
Keywords
- Acetylomics
- Aging
- Elamipretide
- Heart
- Mitochondria
- NMN
- Proteomics
- SS-31