VAT-derived small extracellular vesicles containing miR-295-3p disrupt cardiac autophagy, exacerbating heart failure with preserved ejection fraction in obesity.
Visceral adipose tissue-derived small extracellular vesicles containing miR-295-3p exacerbate HFpEF by disrupting cardiac autophagy, highlighting a novel mechanism of adipocyte-cardiomyocyte crosstalk.
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The present work unveils a mechanism whereby obesity promotes HFpEF progression, emphasizing the role of VAT-heart crosstalk. Specifically, VAT-derived sEVs, miR-295-3p, and the resultant disruption of cardiac autophagy contribute significantly to the pathogenesis of HFpEF.
Pan et al. (Thu,) reported a other. VAT-derived small extracellular vesicles containing miR-295-3p disrupt cardiac autophagy, exacerbating heart failure with preserved ejection fraction in obesity.