UQCRB regulates mitochondrial energy metabolism by promoting COX5 A in atherosclerotic endothelial dysfunction.

ABSTRACT: Mitochondrial dysfunction plays a critical role in the onset and progression of Atherosclerosis (AS). The ubiquinol-cytochrome c reductase binding protein (UQCRB) is an essential subunit of the mitochondrial respiratory chain. The objective of this study was to investigate whether UQCRB improves endothelial dysfunction in AS by upregulating cytochrome c oxidase subunit 5A (COX5A), thereby regulating mitochondrial energy metabolism, reducing inflammation, and preventing apoptosis. To explore the biological role of UQCRB in AS, we found that UQCRB was significantly downregulated in AS, based on bioinformatics analysis and clinical patient data. In vitro, overexpression of UQCRB significantly increased COX5A protein expression in response to oxidized low-density lipoprotein (OX-LDL), enhanced

SUBMITTER: Dai R 

PROVIDER: S-EPMC12552377 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature