Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Aug;37(4):9804.
doi: 10.1007/s11357-015-9804-y. Epub 2015 Jun 23.

Sirtuins, aging, and cardiovascular risks

Affiliations
Review

Sirtuins, aging, and cardiovascular risks

Gaia Favero et al. Age (Dordr). 2015 Aug.

Abstract

The sirtuins comprise a highly conserved family proteins present in virtually all species from bacteria to mammals. Sirtuins are members of the highly conserved class III histone deacetylases, and seven sirtuin genes (sirtuins 1-7) have been identified and characterized in mammals. Sirtuin activity is linked to metabolic control, apoptosis, cell survival, development, inflammation, and healthy aging. In this review, we summarize and discuss the potential mutual relations between each sirtuin and cardiovascular health and the impact of sirtuins on oxidative stress and so age-related cardiovascular disorders, underlining the possibility that sirtuins will be novel targets to contrast cardiovascular risks induced by aging.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Sirtuin 1 mechanism of action against cardiovascular aging. In particular, resveratrol, caloric restriction, or tyrosol upregulate sirtuin 1 expression and activity; in turn, sirtuin 1 can activate FOXOs and eNOS to reduce/block oxidative stress and vasculoreactivity alteration, playing a final important role in counteract cardiovascular aging. (Modified from Luo et al. 2014). eNOS endothelial nitric oxide, FOXO forkhead box O, SIRT1 sirtuin 1
Fig. 2
Fig. 2
Cardiovascular targets modulated by each sirtuins; endothelial cells, vascular smooth muscle cells, and cardiomyocytes might regulate, through different targets, various physiopathological processes. Ang II angiotensin II, AT1P angiotensin II type 1 receptor, eNOS endothelial nitric oxide, FOXO forkhead box O, GDH glutamate dehydrogenase, HIF hypoxia inducible factor, NF-kB nuclear factor kB, Mn-SOD manganese superoxide dismutase, PDE phosphodiesterases, RIP receptor-interacting protein, SIRT sirtuin, TF transcription factors, TNF-α tumor necrosis factor
Fig. 3
Fig. 3
Aging depresses sirtuin activity and increases oxidative stress leading to cardiovascular alterations (a). Upon activation by resveratrol or other chemical activators, each sirtuin might deacetilate several proteins that promote resistance to oxidative stress (b). FOXO forkhead box O, NF-kB nuclear factor kB, Mn-SOD manganese superoxide dismutase, SIRT sirtuin

References

    1. Ahuja N, Schwer B, Carobbio S, Waltregny D, North BJ, Castronovo V, Maechler P, Verdin E. Regulation of insulin secretion by SIRT4, a mitochondrial ADP-ribosyltransferase. J Biol Chem. 2007;282(46):33583–33592. - PubMed
    1. Alcendor RR, Gao S, Zhai P, Zablocki D, Holle E, Yu X, Tian B, Wagner T, Vatner SF, Sadoshima J. Sirt1 regulates aging and resistance to oxidative stress in the heart. Circ Res. 2007;100(10):1512–1521. - PubMed
    1. Alcendor RR, Kirshenbaum LA, Imai S, Vatner SF, Sadoshima J. Silent information regulator 2alpha, a longevity factor and class III histone deacetylase, is an essential endogenous apoptosis inhibitor in cardiac myocytes. Circ Res. 2004;95(10):971–980. - PubMed
    1. Banerjee KK, Ayyub C, Ali SZ, Mandot V, Prasad NG, Kolthur-Seetharam U. dSir2 in the adult fat body, but not in muscles, regulates life span in a diet-dependent manner. Cell Rep. 2012;2(6):1485–1491. - PubMed
    1. Banerjee KK, Ayyub C, Sengupta S, Kolthur-Seetharam U. Fat body dSir2 regulates muscle mitochondrial physiology and energy homeostasis nonautonomously and mimics the autonomous functions of dSir2 in muscles. Mol Cell Biol. 2013;33(2):252–264. - PMC - PubMed