Downregulation of UQCRC1 exacerbates hypoxia-induced mitochondrial damage in H9C2 cardiomyocytes

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Abstract

Ubiquinol cytochrome c reductase core protein I (UQCRC1) is a critical component of mitochondrial proteins, and abnormal expression or dysfunction of UQCRC1 may be associated with the occurrence and progression of certain diseases. Our previous study found significant changes in the content of UQCRC1 protein in myocardial cells in a mouse acute myocardial ischemia model. However, there have been no reports on how changes in UQCRC1 protein content affect mitochondrial function in myocardial cells. In this study, we silenced the UQCRC1 gene in rat myocardial cells under hypoxic conditions using a constructed shRNA expression vector. Experimental techniques such as Hoechst staining system, inverted fluorescence microscopy, electron microscopy, and CCK-8 assay were utilized to observe the apoptosis rate of H9C2 cells and pathological changes in mitochondrial ultrastructure. Additionally, cellular viability, lactate dehydrogenase levels, reactive oxygen species, ATP expression, and mitochondrial membrane potential changes were measured in H9C2 cells to preliminarily elucidate the impact of the UQCRC1 gene on mitochondrial function in rat hypoxic myocardial cells from both morphological and functional aspects. Our study sheds light on the partial mechanisms underlying the occurrence and prognosis of ischemic heart disease cardiomyopathy through the UQCRC1 pathway.

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