TRIM13 prevents cardiomyocyte injury by affecting apoptosis through interacting with CD3D in myocardial infarction

Myocardial infarction (MI) is a common cardiovascular disease with a high risk of sudden death. We aim to develop potential and more effective therapeutic strategies for treating and preventing MI. A mouse model of MI was established, and cardiac tissue sample microarray data and GSE236374 dataset were collected to screen and 120 upregulation and 15 downregulation genes were obtained, and related to T cells and cell immunity. Further obtained 7 key genes, including Cd8b1, Pdcd1, Klrd1, Klrk1, Cd3g, Cd74, and Cd3d, and had high expression in MI mice. The ceRNA regulation network found that protein TRIM13 was upstream of CD3D. In vitro and in vivo knockdown of CD3D relieved the effect of OGD-induced cardiomyocyte apoptosis. TRIM13 interacts with CD3D. Knockdown of TRIM13 promotes CD3D ubiquitination and restores the effect of OGD-induced cardiomyocyte apoptosis through downregulation of CD3D. Knockdown of TRIM13 could relieve cardiomyocyte apoptosis through downregulation of CD3D in MI.