Role of autophagy in atherosclerosis: foe or friend?

Abstract

Athrosclerosis is conceived as a chronic inflammatory status affecting cells from vascular walls. Different mechanisms and pathological features are evident at the onset of atherosclerotic changes via the engaging different cells from the vascular wall and circulatory cells. Attempts are currently focused on the detection of cell compensatory mechanisms against atherosclerotic changes to restore cell function and/or postpone severe vasculitis. Autophagy is an intracellular self-digesting process commonly protrudes exhausted organelles and injured cytoplasmic constituents via double-lipid bilayer membrane vesicles out the target cells. Recent investigations point to the critical and defensive role of autophagy in the vascular cells behavioral function such as endothelial cells and smooth muscle cells against different insults. Autophagy response and related effectors could be modulated in the favor to restore cell function and reduce pro-inflammatory status under pathological conditions. In this review, the recent findings were collected regarding the role of autophagy during atherosclerotic changes. We aimed to answer the question of how autophagy stimulation and/or inhibition could provide a promising effect on developing a sophisticated treatment for AS.

Rapamycin promotes endothelial–mesenchymal transition during stress-induced premature senescence through the activation of autophagy

“…In these reports, the relationship with autophagy is unknown. To date, many preclinical studies on the relationship between autophagy and cardiovascular diseases have been performed [62,63]. From those studies, it has been suggested that autophagy plays a dual role in cardiovascular disease progression, acting in either beneficial or maladaptive ways, depending on the context.…”

The role of TRPV1 channels in atherosclerosis

“…The most important factor underlying atherosclerosis is abnormal lipid metabolism, especially hypercholesterolemia, for which low-density lipoprotein cholesterol (LDL-C) is an acknowledged risk factor. LDL-C enters the vascular intima through damaged endothelial cells and is converted to oxidized low-density lipoprotein cholesterol (ox LDL-C), which can be recognized by the scavenger receptor (SR) of vascular smooth muscle cells (VSMCs) and monocyte-derived macrophages and then engulfed to form foam cells and early lipid streaks [10] (Figure 1). TRPV1 can regulate lipid metabolism, initially by reducing blood lipid levels, and Ma et al, who fed capsaicin to atherosclerotic mice, showed that compared with those in ApoE (−/−) TRPV1 (−/−) mice, the serum total cholesterol and triglyceride levels in apolipoprotein E knockout mice (ApoE (−/−) ) mice were significantly reduced, and lipid accumulation in aortic SMCs was also significantly reduced [11].…”

“…Atherosclerosis is considered to be a chronic inflammatory disease that mainly refers to large myoelastic arteries (e.g., the aorta) and mediumsized myoelastic arteries (e.g., coronary and cerebral arteries) [8].The risk factors for atherosclerosis include hypertension, hyperlipidemia, diabetes, obesity and smoking [9]. The pathogenesis mainly includes endothelial cell injury, lipid deposition, foam cell formation, inflammation, oxidative stress, and SMCs proliferation, among others [10] ( Figure 1).…”

MicroRNA-103 Protects Coronary Artery Endothelial Cells against H2O2-Induced Oxidative Stress via BNIP3-Mediated End-Stage Autophagy and Antipyroptosis Pathways

“…Autophagy has dual effects on AS, a chronic inflammatory disease. Although autophagy can prevent early changes associated with AS by inhibiting inflammatory cells and maintaining the stability of vascular wall cells, it can also aggravate the disease in late AS stage [30].…”