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Curr Drug Targets CNS Neurol Disord 4 , 657665 (2005)

Oxidative stress and protection against reactive oxygen species in the pre-implantation embryo and its surroundings

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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For one thing, there is no evidence that the negative effect reported can be replicated outside of the mouse model used