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Histone deacetylase 4: A therapeutic target for cardiovascular diseases (Review)
Xiaotong Ma1, Ran Wei1, Anni Song2
1College of Rehabilitation Medicine, Shandong University of Traditional Chinese Medicine, Jinan, Shandong 250355, P.R. China.
Insights
Histone deacetylase 4 (HDAC4) plays a key role in cardiovascular diseases (CVD) by influencing inflammation, fibrosis, and apoptosis. Understanding HDAC4
Area of Science:
- Biomedical research
- Cardiovascular science
- Molecular biology
Background:
- Cardiovascular disease (CVD) presents a significant global health challenge.
- Rising incidence and mortality rates necessitate novel therapeutic strategies.
- Histone deacetylase 4 (HDAC4) is emerging as a critical factor in CVD pathogenesis.
Purpose of the Study:
- To review the functional roles of HDAC4 in cardiovascular diseases.
- To examine the impact of pharmacological agents and physical exercise on HDAC4 expression.
- To highlight the need for further research into HDAC4's molecular mechanisms in CVD.
Main Methods:
- Literature review of studies on HDAC4 and CVD.
- Analysis of HDAC4's regulation of pathophysiological processes (inflammation, fibrosis, apoptosis).
- Examination of therapeutic interventions affecting HDAC4 expression.
Main Results:
- HDAC4 influences cardiac hypertrophy, hypertension, and atherosclerosis.
- HDAC4 modulates key processes including inflammation, fibrosis, and apoptosis in CVD.
- Pharmacological agents and physical exercise can affect HDAC4 expression.
Conclusions:
- HDAC4 is a significant regulator in the development and progression of CVD.
- Further elucidation of HDAC4's molecular mechanisms is crucial for clinical applications.
- Targeting HDAC4 may offer new avenues for CVD diagnosis and treatment.
Abstract:
Cardiovascular disease (CVD) is a major global health threat, as its incidence and mortality rates continue to rise, highlighting the urgent need for effective therapeutic strategies. Histone deacetylase 4 (HDAC4), a member of class IIa HDACs, has attracted increasing attention in recent years for its role in CVD. Studies have shown that HDAC4 can influence the development and progression of CVD such as cardiac hypertrophy, hypertension and atherosclerosis by regulating key pathophysiological processes including inflammation, fibrosis and apoptosis. The present review focuses on the functional roles of HDAC4 in CVD and examines the effects of pharmacological agents and physical exercise on its expression. Future research should further elucidate the molecular mechanisms underlying HDAC4's involvement in CVD to provide new theoretical foundations for clinical diagnosis and treatment.
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