Effect of HDAC4 Regulation of β-Catenin Signaling Pathway on Cardiac Injury in Spontaneously Hypertensive Rats and Its Mechanism

Histone deacetylase 4 (HDAC4) is highly expressed in patients with essential hypertension and is closely related to myocardial injury. Therefore, this study aims to explore the effects and mechanisms of HDAC4 on cardiac injury in spontaneously hypertensive rats, with the aim of providing new directions for the diagnosis and treatment of hypertensive myocardial disease. Compared with those in the WKY group, the blood pressure, myocardial injury markers, myocardial cell apoptosis rate, cleaved-caspase9 protein, TNF-α, HDAC4 mRNA, HDAC4 protein, IL-6, cleaved-caspase3 protein, MDA, β-catenin protein, IL-1β, and Wnt3a protein levels in the SHR group significantly increased ( P < 0.05), while LVEF and SOD levels significantly decreased ( P < 0.05); interfering with HDAC4 expression can reduce the cardiomyocyte apoptosis rate, cleaved-caspase9 protein, TNF-α, HDAC4 mRNA, HDAC4 protein, IL-6, cleaved-caspase3 protein, MDA, β-catenin protein, IL-1β, and Wnt3a protein levels, and increase LVEF and SOD levels; overexpression of HDAC4 has the opposite effect. HDAC4 may play a role in regulating cardiac injury in SHR rats by regulating β-catenin signaling pathway.