AI Article Synopsis
- The study examined how aging affects protein levels and acetylation in mouse hearts, focusing on changes associated with aging.
- It tested two drugs, elamipretide and NMN, which showed modest success in reversing these age-related protein changes while causing some additional effects.
- Findings highlighted that increased protein acetylation mainly impacted mitochondrial functions and identified crucial changes in proteins linked to heart function as we age.
Article 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9213586 | PMC |
| http://dx.doi.org/10.1007/s11357-022-00564-w | DOI Listing |
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