Autophagy of monocytes attenuates the vulnerability of coronary atherosclerotic plaques

Abstract

Autophagy of PBMs is involved in the pathogenesis of plaque vulnerability and subsequent plaque rupture. Enhancing the autophagy of PBMs may be a new therapeutic target for stabilizing atherosclerotic plaques.

Endoplasmic reticulum stress‐dependent autophagy inhibits glycated high‐density lipoprotein‐induced macrophage apoptosis by inhibiting CHOP pathway

“…17 Recently, multiple lines of evidence have revealed that both ER stress and autophagy are implicated in the pathogenesis of atherosclerotic plaque vulnerability and subsequent plaque rupture. 12,18,19 However, the interaction of ER stress and autophagy in the progression of atherosclerosis induced by hyperglycaemia is currently unknown. In the present study, we investigated the roles of ER stress and autophagy in gly-HDL-induced macrophage apoptosis and the crosstalk between them in atherosclerosis.…”

Resveratrol protects neuronal cells from isoflurane‑induced inflammation and oxidative stress‑associated death by attenuating apoptosis via Akt/p38 MAPK signaling

“…With high anesthetic efficacy, inhalation anesthetics, which allow for easy control of the depth of anesthesia, have been widely applied in a clinical setting for >170 years (1,2). In the USA, the number of individuals receiving general anesthesia reaches 40 million each year.…”

Lower AMP-activated protein kinase level is associated with the vulnerability of coronary atherosclerotic plaques by attenuating the expression of monocyte autophagy

“…In the present study, we found that AMPK activity and autophagy of monocytes were significantly decreased in ACS patients compared with those in the SAP and control groups. As described in our previous study, autophagy of PBMs in patients with coronary heart disease increases the vulnerability of atherosclerotic plaques [5]. AMPK can regulate autophagy by activating autophagic regulatory protein in the initial step of autophagy-mediated degradation [10].…”

“…Our data showed that the expression levels of beclin-1 and ATG7 were low in circulating monocytes. Autophagy may be more likely to contribute toward attenuating the vulnerability of atherosclerotic plaques [5]. Monocytes are the key immune cells that play a significant role in atherosclerotic plaques.…”

“…Matsui et al [4] found that autophagy was protective during ischemia. Recently, Zhao et al [5], in our laboratory, indicated that autophagy of peripheral blood monocytes (PBMs) participates in the pathogenesis of plaque vulnerability and the subsequent plaque rupture.…”