Key result
Interfering with HDAC4 expression in spontaneously hypertensive rats significantly reduced cardiomyocyte apoptosis and inflammatory markers while increasing LVEF and SOD levels (P < 0.05).
Why the study?
HDAC4 is highly expressed in essential hypertension and closely linked to myocardial injury, but its effects and mechanisms in spontaneously hypertensive rats remain to be explored.
Does HDAC4 regulation improve cardiac injury in spontaneously hypertensive rats?
Does HDAC4 regulation improve cardiac injury in spontaneously hypertensive rats?
HDAC4 regulation may protect against hypertensive myocardial injury by modulating the β-catenin signaling pathway, offering a potential new therapeutic target.
HDAC4 inhibition may attenuate hypertensive myocardial injury in rats; leaves open clinical translation and therapeutic targeting.
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.
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Li et al. (2025) studied Hypertensive myocardial disease. HDAC4 interference vs. WKY group / SHR control was evaluated on Myocardial injury markers, apoptosis rate, LVEF, and SOD levels (p=< 0.05). Interfering with HDAC4 expression in spontaneously hypertensive rats significantly reduced cardiomyocyte apoptosis and inflammatory markers while increasing LVEF and SOD levels (P < 0.05).
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