Corrigendum to “Negative feedback regulation between microRNA let-7g and LOX-1 mediated hypoxia-induced PASMCs proliferation” [Biochem. Biophys. Res. Comm. 488 (4) (2017) 655–663]

Zhang, Weifang; Zhu, Tiantian; Xiong, You-Wen; Xiong, Aizhen; Ge, Xinlan; Hu, Chang-Ping; Zhang, Zheng

doi:10.1016/j.bbrc.2017.08.080

Cited by 1 publication

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A second example is the miRNA let‐7 g, a member of the let‐7 family of miRNAs, which is closely associated with the development of cardiovascular disease. Ox‐LDL and hypoxia increase LOX‐1 expression and decrease let‐7 g expression in rat and human artery VSMCs, respectively, while let‐7 g mimics decrease LOX‐1 expression via direct binding to the 3′‐untranslated region (3′‐UTR) of the LOX‐1 mRNA, suggesting a negative feedback regulation between LOX‐1 and let‐7 g. Furthermore, when ApoE –/– mice were fed a high‐fat diet, enhanced expression of LOX‐1 was observed in the aorta, whereas the upregulation of LOX‐1 was inhibited by treatment with let‐7 g mimics . Likewise, an increase of LOX‐1 expression, foam cell formation, and lipid accumulation in ApoE –/– mice fed a high‐fat fed were all abrogated after the administration of miR‐98 mimics .…”

Section: Regulation Of Lox‐1mentioning

confidence: 99%

Targeting LOX‐1 in atherosclerosis and vasculopathy: current knowledge and future perspectives

Tian

Ogura

Little

et al. 2018

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

LOX-1 (lectin-like oxidized low-density lipoprotein receptor-1; also known as OLR1) is the dominant receptor that recognizes and internalizes oxidized low-density lipoproteins (ox-LDLs) in endothelial cells. Several genetic variants of LOX-1 are associated with the risk and severity of coronary artery disease. The LOX-1-ox-LDL interaction induces endothelial dysfunction, leukocyte adhesion, macrophage-derived foam cell formation, smooth muscle cell proliferation and migration, and platelet activation. LOX-1 activation eventually leads to the rupture of atherosclerotic plaques and acute cardiovascular events. In addition, LOX-1 can be cleaved to generate soluble LOX -1 (sLOX-1), which is a useful diagnostic and prognostic marker for atherosclerosis-related diseases in human patients. Of therapeutic relevance, several natural products and clinically used drugs have emerged as LOX-1 inhibitors that have antiatherosclerotic actions. We hereby provide an updated overview of role of LOX-1 in atherosclerosis and associated vascular diseases, with an aim to highlighting the potential of LOX-1 as a novel theranostic tool for cardiovascular disease prevention and treatment.

show abstract

Section: Regulation Of Lox‐1mentioning

confidence: 99%