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Oxidative mtDNA damage elevates 8-OHdG expression, potentially leading to NLRP3/NLRP6 imbalance, Caspase-1 activation, and release of IL-1 and IL-18 [16]

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Figure 4 Myocardial hypertrophy and fibrosis TMAO significantly increased the mRNA and protein levels of the hypertrophic markers atrial natriuretic peptide (ANP) and -myosin heavy chain (-MHC), causing myocardial hypertrophy and fibrosis ( Exacerbation of mitochondrial dysfunction The accumulation of TMAO in cardiac tissue led to disturbed energy metabolism and impaired myocardial function ( T-tubule remodeling in cardiomyocytes TMAO disturbed myocardial excitation-contraction coupling by inducing Ca 2+ dysfunction ( 2+ channels (VGCCs), located predominantly on the T-tubule membrane, and type 2 ryanodine receptor (RyR2), a Ca 2+ -release channel located on the sarcoplasmic reticulum ( 2+

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