Retraction for Lv et al., ABHD5 protects cardiac function in alcoholic cardiomyopathy via HDAC4-NT to inhibit...

Area of Science:

• Cardiology
• Molecular Biology
• Toxicology

Background:

• Excessive alcohol intake is a leading cause of alcoholic cardiomyopathy (ACM), characterized by impaired cardiac function.
• The molecular mechanisms underlying ACM, particularly the role of specific proteins and signaling pathways, require further elucidation.

Purpose of the Study:

• To investigate the role of Abhydrolase Domain Containing 5 (ABHD5) in the pathogenesis of alcoholic cardiomyopathy (ACM).
• To explore the involvement of the histone deacetylase 4 (HDAC4) and CaM-CaMKII/MEF2 signaling pathway in ABHD5-mediated regulation of ACM.

Main Methods:

• Establishment of Wistar rat models for ACM and in vitro H9C2 cardiomyocyte models treated with alcohol.
• Assessment of cardiac function, myocardial fibrosis, cardiomyocyte apoptosis, and oxidative stress.
• Analysis of ABHD5 mRNA and protein expression, and mechanistic studies involving HDAC4 and the CaM-CaMKII/MEF2 pathway.

Main Results:

• ABHD5 mRNA and protein expression were significantly reduced in ACM models.
• Overexpression of ABHD5 (oe-ABHD5) repressed myocardial hypertrophy and fibrosis in ACM rats.
• ABHD5 overexpression reduced apoptosis and oxidative stress in H9C2 cells, mediated via HDAC4 inhibition of the CaM-CaMKII/MEF2 axis.

Conclusions:

• ABHD5 plays a protective role against alcohol-induced cardiac injury.
• ABHD5 mitigates cardiac hypertrophy, myocardial fibrosis, cardiomyocyte apoptosis, and oxidative stress in ACM.
• Targeting ABHD5 may represent a therapeutic strategy for alcoholic cardiomyopathy.