id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-328846-q52fjx99	Okuno, Keisuke	Targeting Molecular Mechanism of Vascular Smooth Muscle Senescence Induced by Angiotensin II, A Potential Therapy via Senolytics and Senomorphics	2020-09-09		.txt	text/plain	7202	407	35	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. Accordingly, EGFR, mitochondrial fission/Drp1 and ER stress likely play upstream roles in AngII-induced vascular senescence and SASP thus contributing to RAS-mediated pathophysiology in CVDs (Figure 4) . Mitochondrial fission and ER stress likely play upstream roles in AngII-induced vascular senescence and SASP contributing to RAS-mediated pathophysiology in CVDs. In addition to the molecular mechanisms illustrated in Figure 2 , mitochondrial fission and ER stress are enhanced under chronic RAS activation contributing to VSMC senescence [6] . Mitochondrial fission and ER stress likely play upstream roles in AngII-induced vascular senescence and SASP contributing to RAS-mediated pathophysiology in CVDs. In addition to the molecular mechanisms illustrated in Figure 2 , mitochondrial fission and ER stress are enhanced under chronic RAS activation contributing to VSMC senescence [6] .	./cache/cord-328846-q52fjx99.txt	./txt/cord-328846-q52fjx99.txt