Why the study?
AMPK regulates cellular energetics and may exert non-metabolic effects, but its specific cardiac roles remain to be deciphered without peripheral organ confounding.
Population
Cardio-specific inducible Ampkα2 gene deletion mouse model
Comparison
Cardio-specific Ampkα2 deficiency vs controls in male and female mice, and ovariectomy in females
Design
Preclinical animal study
Key result
Cardio-specific Ampkα2 deletion in mice led to progressive left ventricular systolic dysfunction, cardiac fibrosis, and mitochondrial cardiolipin remodeling in males, but not in females.
Authors
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May warrant sex-specific AMPK targeting in HF; leaves open human translation and sex-stratified trials.
Absolute Event Rate: 71.1% vs 78.3%
p-value: p=<0.05
AMPK plays a sex-specific role in cardiac mitochondrial function and fibrosis, which may have clinical implications for using AMPK activators to treat heart failure.
Grimbert et al. (2021) studied Cardiac dysfunction and fibrosis. Cardio-specific Ampkα2 deletion vs. Control mice (Ampkα2 f/f treated with tamoxifen) was evaluated on Left ventricular ejection fraction in males at 16 weeks (p=<0.05). Cardio-specific Ampkα2 deletion in mice led to progressive left ventricular systolic dysfunction, cardiac fibrosis, and mitochondrial cardiolipin remodeling in males, but not in females.
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