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Resistance exercise upregulates Irisin expression and suppresses myocardial fibrosis following myocardial infarction via activating AMPK‐Sirt1 and inactivating TGFβ1‐Smad2/3
Resistance exercise increases Irisin levels and reduces heart scarring after heart attack by activating energy regulation and blocking scar-forming pathways
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Abstract
Resistance exercise increased Fndc5 mRNA levels and improved cardiac function in mice with myocardial infarction.
- Resistance exercise reduced oxidative stress, apoptosis, and myocardial fibrosis in infarcted hearts.
- Fndc5 knockout diminished the protective effects of resistance exercise on cardiac health.
- AICAR and recombinant human Irisin intervention activated the AMPK-Sirt1 pathway in cardiac fibroblasts.
- The activation of the AMPK-Sirt1 pathway and inhibition of the TGFβ1-Smad2/3 pathway were observed with rhIRISIN treatment.
- Effects of rhIRISIN were partially reduced by Sirt1 inhibition, indicating a potential pathway involvement.
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