TMAO activates signaling pathways such as TGF-β1/Smad3 and p65 NF-κΒ, leading to a decrease in energy metabolism and mitochondrial function, and impairs the tricarboxylic acid (TCA) cycle, ultimately adversely affecting myocardial contractile function and intracellular calcium processing, and consequently triggering cardiac hypertrophy and myocardial fibrosis [1,20,22]. This evidence concerns the gene TGFB1 and Myocardial fibrosis.