Key result
OGA overexpression rescues severe dilated cardiomyopathy and premature death caused by myocardial OGT.
Why the study?
Failing myocardium is marked by increased O-GlcNAcylation, but whether excessive O-GlcNAcylation contributes to cardiomyopathy and heart failure is unknown.
Does excessive O-GlcNAcylation cause cardiomyopathy and does its attenuation protect against heart failure in mouse models?
Population
Transgenic mouse models with myocardial overexpression of OGT and OGA
Comparison
OGT and OGA transgenic mice versus wild-type littermate controls and OGT/OGA interbred mice
Design
Preclinical study using transgenic mouse models
Authors
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O-GlcNAcylation may link metabolic stress to cardiac protein modification in experimental HF; leaves open human relevance.
Does excessive O-GlcNAcylation cause cardiomyopathy and does its attenuation protect against heart failure in mouse models?
Excessive O-GlcNAcylation causes cardiomyopathy through defective mitochondrial energetics, suggesting OGA activation as a potential therapeutic target for heart failure.
Umapathi et al. (2021) studied Cardiomyopathy and heart failure. Myocardial overexpression of OGT and OGA vs. Wild-type littermate controls was evaluated on Development of dilated cardiomyopathy, ventricular arrhythmias, and premature death. Myocardial overexpression of OGT caused severe dilated cardiomyopathy, ventricular arrhythmias, and premature death, which was rescued by OGA overexpression.
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