Role of mitochondrial ribosomal protein L7/L12 (MRPL12) in diabetic ischemic heart disease

Myocardial infarction (MI) is a significant cause of death in diabetic patients. Growing evidence suggests that mitochondrial dysfunction contributes to heart failure in diabetes. However, the molecular mechanisms of mitochondrial dysfunction mediating heart failure in diabetes are still poorly understood. The current study aimed to investigate the role of mitochondrial ribosomal protein L7/L12 (MRPL12) in human heart. Mitochondrial oxygen consumption rate and membrane potential was determined using Seahorse analysis and confocal microscopy respectively. Data was analyzed by using the mean of the groups was compared using a student t-test (for 2 groups) and ANOVA, followed by a Tukey test (for >2 groups). We found increased MRPL12 levels in heart tissue samples of diabetic patients with ischemic heart disease compared to non-diabetic patients. With the overexpression of MRPL12 under hyperglycemic conditions, the level of oxidative phosphorylation (OXPHOS) was found downregulated, but cellular ATP and human cardiomyocyte cell death remained unchanged, However, there was notable impairment in mitochondrial membrane potential (MMP) in hyperglycemia condition, along with changes in basal respiration oxygen consumption rate (OCR) and maximal respiratory capacity OCR. Overall, our results suggest that MRPL12 may have a compensatory role in the diabetic myocardium with ischemic heart disease, suggesting that MRPL12 may implicate in the pathophysiology of MI in diabetes.