Key result
Transiently increased cardiomyocyte O-GlcNAcylation prior to pressure overload exacerbated adverse cardiac remodeling, including decreased cardiac function, increased hypertrophy, and fibrosis.
Why the study?
Understanding of the mechanisms underlying metabolic memory remains limited, prompting the hypothesis that transiently increased cardiomyocyte O-GlcNAcylation exacerbates adverse cardiac remodeling following subsequent pressure-overload.
Does transiently increased cardiomyocyte O-GlcNAcylation exacerbate adverse cardiac remodeling after subsequent pressure-overload in mice?
Population
Inducible cardiomyocyte specific, dominant-negative O-GlcNAcase (dnOGAh) mice and single transgenic littermate controls
Comparison
Transient O-GlcNAc induction (ON/OFF) vs control (Con) followed by TAC or Sham surgery
Design
Preclinical animal study
Authors
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Should not yet change practice; leaves open whether O-GlcNAc memory drives lasting diabetic cardiomyopathy risk.
Does transiently increased cardiomyocyte O-GlcNAcylation exacerbate adverse cardiac remodeling after subsequent pressure-overload in mice?
Transiently elevated cardiomyocyte O-GlcNAcylation exacerbates future pressure overload-induced cardiac remodeling, providing a molecular basis for 'metabolic memory' in diabetic heart disease.
Chang et al. (2025) studied Pressure overload-induced cardiac remodeling. Transient increase in cardiomyocyte protein O-GlcNAcylation vs. Single transgenic littermate controls (Con) was evaluated on Cardiac remodeling (hypertrophy, fibrosis, cardiac function). Transiently increased cardiomyocyte O-GlcNAcylation prior to pressure overload exacerbated adverse cardiac remodeling, including decreased cardiac function, increased hypertrophy, and fibrosis.
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