@entity19812 alleviates post-infarction @entity299 by up-regulating autophagy through XXXX inhibition.

@entity1 @entity39915 @entity409 @entity10407 @entity3736 @entity519 @entity299 @entity19812 @entity583 @entity855
UNASSIGNED: @entity583 ( @entity583 ), which is characterized by chamber dilation and @entity409 , is associated with substantially higher mortality. We investigated the effects and underlying mechanisms of @entity19812 on post-infarction @entity299 . @entity583 was constructed by left anterior descending coronary artery ligation. In vitro, cultured neonatal cardiomyocytes subjected to simulated @entity583 were used to probe mechanism. @entity19812 significantly improved cardiac function, decreased cardiac enzyme and inflammatory cytokines release after @entity583 . Enhanced autophagic flux as indicated by more autophagosomes puncta, less accumulation of aggresomes and @entity10407 in the neonatal cardiomyocytes after @entity519 was observed in the @entity19812 pre-treatment group. Western blot analysis also demonstrated that @entity19812 up-regulated autophagy in the cardiomyocytes subjected to simulated @entity583 . Furthermore, @entity19812 increased mitochondrial membrane potential, @entity855 content, @entity3736 synthase activity and complexes I/II/III/IV/V activities in the cardiomyocytes subjected to simulated @entity583 . Interestingly, @entity1 sterile 20-like kinase 1 ( @entity39915 ) knockout abolished the protective effects of @entity19812 administration. @entity19812 enhances cardiac function, reduces cardiac enzyme and inflammatory markers release after @entity583 . The protective effects of @entity19812 are associated with up-regulation of autophagy and improvement of mitochondrial biogenesis through @entity39915 inhibition.
