Targeting Molecular Mechanism of Vascular Smooth Muscle Senescence Induced by Angiotensin II, A Potential Therapy via Senolytics and Senomorphics
Genre
Journal articleDate
2020-09-09Author
Okuno, KeisukeCicalese, Stephanie

Elliott, Katherine J.
Kawai, Tatsuo
Hashimoto, Tomoki
Eguchi, Satoru

Group
Cardiovascular Research Center (Temple University)Department
PhysiologyPermanent link to this record
http://hdl.handle.net/20.500.12613/4165
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http://doi.org/10.3390/ijms21186579Abstract
Cardiovascular disease (CVD) is a prevalent issue in the global aging population. Premature vascular aging such as elevated arterial stiffness appears to be a major risk factor for CVD. Vascular smooth muscle cells (VSMCs) are one of the essential parts of arterial pathology and prone to stress-induced senescence. The pervasiveness of senescent VSMCs in the vasculature increases with age and can be further expedited by various stressing events such as oxidative stress, mitochondria dysfunction, endoplasmic reticulum stress, and chronic inflammation. Angiotensin II (AngII) can induce many of these responses in VSMCs and is thus considered a key regulator of VSMC senescence associated with CVD. Understanding the precise mechanisms and consequences of senescent cell accumulation may uncover a new generation of therapies including senolytic and senomorphic compounds against CVD. Accordingly, in this review article, we discuss potential molecular mechanisms of VSMC senescence such as those induced by AngII and the therapeutic manipulations of senescence to control age-related CVD and associated conditions such as by senolytic.Citation
Okuno K, Cicalese S, Elliott KJ, Kawai T, Hashimoto T, Eguchi S. Targeting Molecular Mechanism of Vascular Smooth Muscle Senescence Induced by Angiotensin II, A Potential Therapy via Senolytics and Senomorphics. International Journal of Molecular Sciences. 2020; 21(18):6579.Citation to related work
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International Journal of Molecular Sciences, Vol. 21, Issue 18ADA compliance
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http://dx.doi.org/10.34944/dspace/4147