PYGM Protects Against Myocardial Infarction by Enhancing Glycogenolysis and Facilitating Autophagic Flux
Authors' conclusion
PYGM safeguards against MI-induced myocardial injury by stimulating glycogenolysis and promoting autophagic flux, thus preserving myocardial energy homeostasis.
Study context
- Population
- Patients with myocardial infarction (MI) (cardiac tissue and plasma) and mice with MI
- Comparison
- PYGM deficiency and AAV-mediated PYGM replenishment in mice with MI
Main finding
As reported in the abstract
- Circulating and cardiac PYGM levels significantly decreased in patients with MI, associated with impaired cardiac function
- Loss of PYGM significantly exacerbated MI-induced cardiac dysfunction and damage in mice; PYGM replenishment profoundly reversed these effects
- PYGM enhanced glycogenolysis by activating glycolysis and the pentose phosphate pathway, improving cardiac energy homeostasis and mitigating oxidative stress
- PYGM improved MI-induced autophagic flux obstacles and alleviated cardiac damage by suppressing Thbs1 expression
- Genetic deficiency or pharmacological blockage of autophagy attenuated PYGM's protective effects; cardiac-specific Thbs1 knockdown improved MI-induced dysfunction and damage in PYGM-null mice
Original publication
PYGM Protects Against Myocardial Infarction by Enhancing Glycogenolysis and Facilitating Autophagic Flux. Circulation. Published 24 September 2025. doi:10.
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