2014
DOI: 10.1016/j.atherosclerosis.2014.04.028
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Ox-LDL induces endothelial cell apoptosis via the LOX-1-dependent endoplasmic reticulum stress pathway

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Cited by 87 publications
(63 citation statements)
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“…Previous studies have focused on ox-LDL-induced apoptosis in VSMCs, [38][39][40] endothelial cells [41][42][43][44] and EPCs. 45 The differences in oxidative status, concentration and the treatment time of ox-LDL as well as cell species might account for the different effects of our ] i measurement.…”
Section: Discussionmentioning
confidence: 99%
“…Previous studies have focused on ox-LDL-induced apoptosis in VSMCs, [38][39][40] endothelial cells [41][42][43][44] and EPCs. 45 The differences in oxidative status, concentration and the treatment time of ox-LDL as well as cell species might account for the different effects of our ] i measurement.…”
Section: Discussionmentioning
confidence: 99%
“…NADPH oxidases are the primary enzymes responsible for inducing ROS production in the vascular system. Studies of endothelial cells and aortic smooth muscle cells treated with ox-LDL and 7-ketocholesterol, respectively, have shown that NADPH oxidase mediates ER stress and apoptosis (46,47), whereas probucol, a ROS scavenger, can protect human umbilical vein endothelial cells from injury induced by hypoxia/reoxygenation by inhibiting CHOP upregulation (48). In addition, oxidative stress also resulted from excessive decrease in activities of antioxidative enzymes, such as…”
Section: Hdl From Ms Patients Induces Oxidative Stress and Chop-mediamentioning
confidence: 99%
“…ERS first increases insulin resistance, and then elevates cholesterol/triglyceride levels, thereby contributing to endothelial dysfunction (Kujiraoka et al, 2013). Moreover, Hong et al used human umbilical vein endothelial cells and discovered that Ox-LDL induces endothelial cell apoptosis via the LOX-1-dependent ERS pathway, and further causes endothelial dysfunction, an initial alteration of atherosclerosis (Hong et al, 2014). Other studies also identified the effects of ERS in endothelial dysfunction (Chaube et al, 2012;.…”
Section: Fundamental Mechanisms P a T H O L O G I C A L E X A M I N Amentioning
confidence: 99%
“…Meanwhile, ERS also induces the expression of VLDLR in HL-1 cells, indicating that there is a positive feedback loop, i.e., the hypoxia-induced increase in VLDLR results in ERS, which in turn promotes the expression of the VLDLR (Perman et al, 2011). Hong and colleagues discovered that ox-LDL induces endothelial dysfunction and apoptosis via the LOX-1/ERS pathway (Hong et al, 2014), while Ishiyama et al recently demonstrated that palmitic acid causes upregulation of LOX-1 via activation of the ERS response (Ishiyama et al, 2011). These findings suggest that there may be a positive feedback loop between ERS and LOX-1 expression.…”
Section: ! 19mentioning
confidence: 99%
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