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Articles Published Processes
6/15/2026 8:38:38 AM | Browse: 2 | Download: 0
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Received |
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2025-12-05 00:41 |
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Peer-Review Started |
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2025-12-05 08:43 |
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First Decision by Editorial Office Director |
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2026-01-08 08:08 |
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Return for Revision |
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2026-01-08 08:08 |
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Revised |
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2026-01-12 09:38 |
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Publication Fee Transferred |
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Second Decision by Editor |
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2026-02-02 02:42 |
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Second Decision by Editor-in-Chief |
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Final Decision by Editorial Office Director |
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2026-02-03 00:40 |
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Articles in Press |
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2026-02-03 00:40 |
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Edit the Manuscript by Language Editor |
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Typeset the Manuscript |
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2026-06-01 23:51 |
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Publish the Manuscript Online |
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2026-06-15 08:38 |
| ISSN |
2220-6124 (online) |
| Open Access |
This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ |
| Copyright |
Diabetic kidney disease is increasingly understood as a disorder shaped not only by metabolic and inflammatory injury but also by gut microbial dysbiosis that amplifies renal fibrotic signalling. Song et al demonstrate that trimethylamine N-oxide (TMAO), generated from microbial metabolism of dietary methylamines, functions as a potent upstream driver of transforming growth factor-β/Smad activation and tubulointerstitial fibrosis. Their use of fecal microbiota transplantation and microbial trimethylamine-inhibition provides compelling causal evidence linking dysbiosis, elevated TMAO, and renal injury. This editorial contextualizes these findings within emerging gut-kidney mechanisms and underscores the therapeutic potential of microbiota-targeted strategies in modifying the trajectory of diabetic kidney disease. |
| Article Reprints |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
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| Permissions |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
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| Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
| Website |
http://www.wjgnet.com |
| Category |
Nutrition & Dietetics |
| Manuscript Type |
Editorial |
| Article Title |
Trimethylamine N-oxide as a key microbial mediator in the progression of diabetic kidney disease
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| Manuscript Source |
Invited Manuscript |
| All Author List |
Pranjal Kashiv, Manish Ramesh Balwani, Amit Pasari, Khushboo Saxena and Vivek B Kute |
| ORCID |
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| Funding Agency and Grant Number |
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| Corresponding Author |
Vivek B Kute, Professor, Department of Nephrology, Institute of Kidney Diseases and Research Center, Dr HL Trivedi Institute of Transplantation Sciences, Civil Hospital Campus, Ahmedabad 380016, Gujarat, India. drvivekkute@rediffmail.com |
| Key Words |
Trimethylamine N-oxide; Diabetic kidney disease; Gut microbiota; Renal fibrosis; TGF-β/Smad signalling |
| Core Tip |
Diabetic kidney disease is increasingly understood as a disorder shaped not only by metabolic and inflammatory injury but also by gut microbial dysbiosis that amplifies renal fibrotic signalling. Song et al. demonstrate that trimethylamine N-oxide (TMAO), generated from microbial metabolism of dietary methylamines, functions as a potent upstream driver of TGF-β/Smad activation and tubulointerstitial fibrosis. Their use of fecal microbiota transplantation and microbial TMA-inhibition provides compelling causal evidence linking dysbiosis, elevated TMAO, and renal injury. This editorial contextualizes these findings within emerging gut–kidney mechanisms and underscores the therapeutic potential of microbiota-targeted strategies in modifying the trajectory of diabetic kidney disease. |
| Publish Date |
2026-06-15 08:38 |
| 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
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| URL |
https://www.wjgnet.com/2220-6124/full/v15/i2/117355.htm |
| DOI |
https://doi.org/10.5527/wjn.v15.i2.117355 |
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