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Molecular mechanisms of HF progression regulated by TMAO. In cardiomyocytes, TMAO activated TGF-β1/Smad3 pathway and increased expression levels of ANP and β-MHC, which caused myocardial hypertrophy and fibrosis; TMAO decreased energy metabolism and mitochondrial function by inhibiting the activity of pyruvate, leading to myocardial damage; TMAO also negatively affected the intracellular Ca2+ processing and myocardial contraction.
