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
Published online Jun 25, 2026. doi: 10.5527/wjn.v15.i2.117355
| DMB observation | Mechanistic insight | Relevance to diabetic kidney disease |
| Inhibition of CutC/D TMA lyases | Proximal blockade of microbial TMA formation | Lowers the upstream substrate load driving TMAO accumulation |
| Demonstrated activity in human fecal cultures | Effective within complex microbial ecosystems | Applicable even in dysbiotic communities characteristic of diabetes |
| No observed hepatic, renal, or metabolic toxicity | Preserves physiological homeostasis | Suitable for long-term use in chronic disease settings |
| Reduction of TMA-producing taxa | Favourable restructuring of gut microbial composition | Addresses dysbiosis that contributes to DN severity |
| Prevention of fibrotic signalling | Decreases NOX4, pro-inflammatory cytokines, and Smad activation | Slows the trajectory of diabetic kidney injury |
- Citation: Kashiv P, Balwani MR, Pasari A, Saxena K, Kute VB. Trimethylamine N-oxide as a key microbial mediator in the progression of diabetic kidney disease. World J Nephrol 2026; 15(2): 117355
- URL: https://www.wjgnet.com/2220-6124/full/v15/i2/117355.htm
- DOI: https://dx.doi.org/10.5527/wjn.v15.i2.117355