Knockdown of TGFB2 Attenuates Ischemic Heart Failure by Inhibiting Apoptosis.

Abstract

Heart failure (HF) is a clinical syndrome resulting from cardiac overload and injury. The molecular mechanisms underlying ischemic HF remain unclear. Using the GSE116250 and GSE203160 datasets, we screened for differentially expressed genes (DEGs) in ischemic HF, identifying 132 overlapping genes. Through the protein-protein interaction (PPI) network, we screened nine hub genes-SPP1, POSTN, CCN2, FGF7, OGN, BMP2, LUM, TGFB2, and BMP7-that may serve as diagnostic biomarkers for HF. FGF7 and BMP7 expression levels were reduced, while TGFB2, OGN, and CCN2 expression levels were elevated in rat models of left anterior descending coronary artery ligation. Notably, Cell Counting Kit-8 and flow cytometry showed that TGFB2 knockdown promoted viability and inhibited apoptosis in oxygen glucose deprivation-induced H9c2 cells. Western blot analysis further demonstrated that TGFB2 knockdown decreased cleaved Caspase-3/Caspase-3 and Bax protein levels while increasing Bcl-2 protein expression. These findings reveal that TGFB2 knockdown mitigates ischemic HF by suppressing apoptosis, offering novel insights into the fundamental molecular mechanisms underlying HF.