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Wyss-Coray, T

The researchers hypothesized that one or more medications, called antagonists, could inhibit the damaging signaling caused by TGF-B and PI3K/AKT/mTOR/p70 S6K, which converts the VICs from healthy to damaged

doi: 10.1038/s41564-018-0334-0 136 LaichalkLLThorley-LawsonDA

Animal models confirm TMAOs pathogenic role: reducing plasma TMAO slows CKD progression (138), while TMAO accelerates diabetic nephropathy by activating NLRP3 inflammasome, promoting IL-1/IL-18 release, and worsening renal dysfunction/fibrosis (139)