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Review
. 2020 Apr 22;9(4):1035.
doi: 10.3390/cells9041035.

Nicotine in Senescence and Atherosclerosis

Ann Marie Centner  1 , Pradeep G Bhide  2 , Gloria Salazar  1   3
Affiliations
Review

Nicotine in Senescence and Atherosclerosis

Ann Marie Centner et al. Cells. .

Abstract

Cigarette smoke is a known exacerbator of age-related pathologies, such as cardiovascular disease (CVD), atherosclerosis, and cellular aging (senescence). However, the role of nicotine and its major metabolite cotinine is yet to be elucidated. Considering the growing amount of nicotine-containing aerosol use in recent years, the role of nicotine is a relevant public health concern. A number of recent studies and health education sites have focused on nicotine aerosol-induced adverse lung function, and neglected cardiovascular (CV) impairments and diseases. A critical review of the present scientific literature leads to the hypothesis that nicotine mediates the effects of cigarette smoke in the CV system by increasing MAPK signaling, inflammation, and oxidative stress through NADPH oxidase 1 (Nox1), to induce vascular smooth muscle cell (VSMC) senescence. The accumulation of senescent VSMCs in the lesion cap is detrimental as it increases the pathogenesis of atherosclerosis by promoting an unstable plaque phenotype. Therefore, nicotine, and most likely its metabolite cotinine, adversely influence atherosclerosis.

Keywords: ApoE−/−; VSMC; atherosclerosis; cigarette smoke; cotinine; nicotine; senescence.

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Conflict of interest statement

The authors declare no conflicts of interest.

References

    1. Benjamin E.J., Muntner P., Alonso A., Bittencourt M.S., Callaway C.W., Carson A.P., Chamberlain A.M., Chang A.R., Cheng S., Das S.R., et al. Heart Disease and Stroke Statistics-2019 Update: A Report From the American Heart Association. Circulation. 2019;139:e56–e528. doi: 10.1161/CIR.0000000000000659. - DOI - PubMed
    1. Erusalimsky J.D., Kurz D.J. Cellular senescence in vivo: Its relevance in ageing and cardiovascular disease. Exp. Gerontol. 2005;40:634–642. doi: 10.1016/j.exger.2005.04.010. - DOI - PubMed
    1. Childs B.G., Durik M., Baker D.J., van Deursen J.M. Cellular senescence in aging and age-related disease: From mechanisms to therapy. Nat. Med. 2015;21:1424–1435. doi: 10.1038/nm.4000. - DOI - PMC - PubMed
    1. Walters M.S., De B.P., Salit J., Buro-Auriemma L.J., Wilson T., Rogalski A.M., Lief L., Hackett N.R., Staudt M.R., Tilley A.E., et al. Smoking accelerates aging of the small airway epithelium. Respir. Res. 2014;15:94. doi: 10.1186/s12931-014-0094-1. - DOI - PMC - PubMed
    1. Tchkonia T., Zhu Y., van Deursen J., Campisi J., Kirkland J.L. Cellular senescence and the senescent secretory phenotype: Therapeutic opportunities. J. Clin. Invest. 2013;123:966–972. doi: 10.1172/JCI64098. - DOI - PMC - PubMed

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