This paper reviews the recent advances concerning the role of endoplasmic reticulum (ER) stress in the pathogenesis of atherosclerosis and its complications. The ER is the site where all the proteins are formed. Under conditions that impair its function, the ER activates a complex response system known as the unfolded protein response (UPR) to restore its function. It has been reported that ER stress promotes lipogenesis and hepatic lipid accumulation, but the mechanisms remain unclear. The ER stress also leads to abnormal insulin action and promotes hyperglycemia through insulin resistance, stimulation of hepatic glucose production and suppression of glucose disposal. ER stress has also been shown to be associated with inflammation and reactive oxygen species. A link has been found between ER stress and macrophage function in the context of atherosclerosis. In fact, lipid-laden macrophages in atherosclerotic lesions appear to activate ER stress response pathways. Moreover, several studies support the idea that macrophage apoptosis and inflammation contribute to the etiology of atherosclerosis. Further studies are needed to better understand the signalling pathways to explain the role of ER stress in atherosclerosis.
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