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Editorial
Copyright: ©Author(s) 2026.
World J Nephrol. Jun 25, 2026; 15(2): 117355
Published online Jun 25, 2026. doi: 10.5527/wjn.v15.i2.117355
Table 3 Mechanistic and therapeutic insights derived from microbial trimethylamine inhibition[10,14,15]
DMB observation
Mechanistic insight
Relevance to diabetic kidney disease
Inhibition of CutC/D TMA lyasesProximal blockade of microbial TMA formationLowers the upstream substrate load driving TMAO accumulation
Demonstrated activity in human fecal culturesEffective within complex microbial ecosystemsApplicable even in dysbiotic communities characteristic of diabetes
No observed hepatic, renal, or metabolic toxicityPreserves physiological homeostasisSuitable for long-term use in chronic disease settings
Reduction of TMA-producing taxaFavourable restructuring of gut microbial compositionAddresses dysbiosis that contributes to DN severity
Prevention of fibrotic signallingDecreases NOX4, pro-inflammatory cytokines, and Smad activationSlows the trajectory of diabetic kidney injury


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