LRG1 promotes hypoxia-induced cardiomyocyte apoptosis and autophagy by regulating hypoxia-inducible factor-1α

Cardiomyocyte apoptosis and autophagy play important roles in acute myocardial infarction (AMI), but the effect of leucine-rich alpha-2-glycoprotein 1 (LRG1) on the apoptosis and autophagy of H9c2 has not yet been reported. It was found through differential gene analysis and LASSO analysis that LRG1 was the key gene in AMI. In this study, western blot was applied to detect the protein expression of Bax, Bcl2, LC3, p62, LRG1 and hypoxia-inducible factor-1 alpha (HIF-1 alpha); CCK-8 assay was employed to detect cell viability; Annexin V-FITC/PI staining was adopted to evaluate apoptosis, and immunofluorescence assay was applied to detect autophagy. Under hypoxia conditions in H9c2 cells, LRG1 protein levels were increased, the cell activity was decreased, and apoptosis and autophagy were promoted; the downregulated LRG1 significantly enhanced cell viability but inhibited apoptosis and autophagy. When knocking down HIF-1 alpha in the overexpressed LRG1 cells, the effects of LRG1 were reversed under hypoxia condition. In conclusion, LRG1/HIF-1 alpha promoted H9c2 cell apoptosis and autophagy in hypoxia, potentially providing new ideas for the determination and treatment of AMI.

Automated summary

In this study, the authors investigated the role of leucine-rich alpha-2-glycoprotein 1 (LRG1) in the apoptosis and autophagy of H9c2 cells in the context of acute myocardial infarction (AMI). They found that LRG1 promotes apoptosis and autophagy under hypoxic conditions, and the effects can be reversed by downregulating LRG1 or knocking down hypoxia-inducible factor-1 alpha (HIF-1 alpha). This study provides new insights into the potential mechanisms of AMI and suggests LRG1/HIF-1 alpha pathway as a novel target for AMI treatment.