Vascular smooth muscle cell autophagy pathway (VSMC autophagy)

Vascular smooth muscle cell (VSMC) autophagy is a fundamental lysosomal degradation process that maintains vascular wall integrity by recycling damaged proteins and organelles [1]. In healthy arteries, basal autophagy is essential for preserving the VSMC contractile phenotype and protecting cells from oxidative stress and senescence [2]. Dysregulation of this pathway is a hallmark of various cardiovascular diseases; for instance, impaired autophagy contributes to vascular calcification and the progression of atherosclerosis by promoting VSMC apoptosis and phenotypic switching to a synthetic state [3]. Conversely, excessive or "autophagic" cell death can destabilize atherosclerotic plaques, leading to rupture and clinical events like myocardial infarction [4]. Therapeutic strategies often involve modulating this pathway using mTOR inhibitors like sirolimus, which are used in drug-eluting stents to prevent restenosis, or AMPK activators like metformin to restore autophagic flux [5]. However, the dual nature of autophagy as both a survival and death mechanism presents a significant challenge for drug development [2]. Citations: [1] Grootaert MO, et al. (2018) Autophagy. [2] Salabei JK, Hill BG. (2013) Prog Cardiovasc Dis. [3] Osonoi S, et al. (2018) Int J Mol Sci. [4] De Meyer GR, et al. (2015) Arterioscler Thromb Vasc Biol. [5] Jia G, et al. (2017) Front Physiol.

Other names

Autophagy in vascular smooth muscle cellsVSMC autophagic fluxVascular smooth muscle cell macroautophagy

Pharmacological agents modulate the pathway by either inducing autophagy (e.g., via mTOR inhibition or AMPK activation) to promote cell survival and phenotypic stability, or by inhibiting autophagic flux (e.g., via lysosomal acidification blockade) to prevent excessive degradation or cell death.