MiR-32-3p Regulates Myocardial Injury Induced by Microembolism and Microvascular Obstruction by Targeting RNF13 to Regulate the Stability of Atherosclerotic Plaques

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“…In an atherosclerotic plaque model in rats, it was found that the inhibition of miR-32-3p led to higher RNF13 expression, an upregulation of ER stress-related proteins, higher arterial plaque instability, a lower survival rate, and increased pathological lesions in the arterial tissue. These results suggest that RNF13 might be involved in atherosclerotic plaques via its role on ER stress-induced cell apoptosis [72].…”

“…In fact, recent studies have shown that RNF13 gene expression is upregulated in atherosclerotic plaques [70] and downregulated in asthma [71]. Also, Huang et al discovered that the microRNA miR-32-3p regulates the expression of RNF13 [72]. Specifically, the expression of miR-32-3p was downregulated in cells that were treated with oxidized low-density lipoprotein (ox-LDL) and TNF-α to simulate an ER stress model, as observed in atherosclerosis [72].…”

“…Also, Huang et al discovered that the microRNA miR-32-3p regulates the expression of RNF13 [72]. Specifically, the expression of miR-32-3p was downregulated in cells that were treated with oxidized low-density lipoprotein (ox-LDL) and TNF-α to simulate an ER stress model, as observed in atherosclerosis [72]. Under the same conditions, RNF13 mRNA expression and protein abundance were upregulated [72].…”

“…Specifically, the expression of miR-32-3p was downregulated in cells that were treated with oxidized low-density lipoprotein (ox-LDL) and TNF-α to simulate an ER stress model, as observed in atherosclerosis [72]. Under the same conditions, RNF13 mRNA expression and protein abundance were upregulated [72]. In addition, ectopic expression of RNF13 in the presence of ox-LDL and TNF-α led to an increase in stress-induced apoptosis [72].…”

“…In addition, ectopic expression of RNF13 in the presence of ox-LDL and TNF-α led to an increase in stress-induced apoptosis [72]. Interestingly, bioinformatics analysis revealed that miR-32-3p was also downregulated in patients with acute myocardial infarction [72].…”