Key result
AMPK activation with AICAR improves diastolic function and reduces fibrosis in female but not male mice.
Why the study?
The aging heart develops diastolic dysfunction because of increased collagen deposition, prompting attempts to reduce collagen expression in the old heart by activating AMPK using AICAR.
Does AICAR improve diastolic function and reduce cardiac fibrosis in aging mice?
Does AICAR improve diastolic function and reduce cardiac fibrosis in aging mice?
AMPK activation with AICAR shows sex-specific benefits, improving diastolic function and reducing fibrosis in aging female but not male mice.
Sex-specific AMPK benefits in female mice warrant caution against human translation; leaves open clinical relevance of AICAR.
The aging heart develops diastolic dysfunction because of increased collagen deposition. We attempted to reduce collagen expression in the old heart by activating AMPK using AICAR. An improvement of diastolic function and reduction of cardiac fibrosis was found only in the female heart and correlated with decreased procollagen expression and increased degradation of the transcription factor Gli1. Male hearts display blunted AICAR-dependent AMPK activation and therefore this treatment had no benefits for the male mice.
No takes yet. Share an insight, caveat, or question.
Angelini et al. (2022) studied Aging heart with diastolic dysfunction and cardiac fibrosis. AICAR was evaluated on Diastolic function and cardiac fibrosis. Activating AMPK using AICAR improved diastolic function and reduced cardiac fibrosis in female mice, but provided no benefits for male mice due to blunted AMPK activation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: