ArticleCommunications biology2024
Deficiency of flavin-containing monooxygenase 3 protects kidney function after ischemia-reperfusion in mice.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Cardiovascular-kidney-metabolic syndrome through the lens of gut‑derived uremic toxins.Gut microbes · 2026Review
- Gut Microbiota and Their Metabolites in Acute Kidney Injury: Classification, Mechanisms, and Therapeutic Potential.Metabolites · 2026Review
- PARKIN overexpression confers cardioprotection via suppressing the mtDNA-cGAS-STING axis in myocardial ischemia/reperfusion injury.Basic research in cardiology · 2026Article
- [Mechanisms of gutZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Trimethylamine-N-oxide: the microbial cue in immune-mediated disorders.Trends in endocrinology and metabolism: TEM · 2026Review
- Targeting gut-liver-kidney axis: microbiota-derived metabolites and therapeutic implications.Cell communication and signaling : CCS · 2026Review
- Adipocyte FMO3-derived TMAO induces WAT dysfunction and metabolic disorders by promoting inflammasome activation in ageing.Nature communications · 2025Article
- CUGBP Elav-like family member 4 promotes cardiac remodeling through Inhibition of FMO2.BMC cardiovascular disorders · 2025Article
- Medium from human iPSC-derived primitive macrophages promotes adult cardiomyocyte proliferation and cardiac regeneration.Nature communications · 2025Article
- Role of NAD metabolism-related genes in diabetic nephropathy: subtype classification, biomarker identification, and association with renal function.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- Alterations in gut-kidney axis indicators and TMAO-related biomarkers in elderly patients with hypertensive nephropathy.Frontiers in medicine · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
The kidney is vulnerable to ischemia and reperfusion (I/R) injury that can be fatal after major surgery. Currently, there are no effective treatments for I/R-induced kidney injury. Trimethylamine N-oxide (TMAO) is a gut-derived metabolite linked to many diseases, but its role in I/R-induced kidney injury remains unclear. Here, our clinical data reveals an association between preoperative systemic TMAO levels and postoperative kidney injury in patients after post-cardiopulmonary bypass surgery. By genetic deletion of TMAO-producing enzyme flavin-containing monooxygenase 3 (FMO3) and dietary supplementation of choline to modulate TMAO levels, we found that TMAO aggravated acute kidney injury through the triggering of endoplasmic reticulum (ER) stress and worsened subsequent renal fibrosis through TGFβ/Smad signaling activation. Together, our study underscores the negative role of TMAO in I/R-induced kidney injury and highlights the therapeutic potential through the modulation of TMAO levels by targeting FMO3, thereby mitigating acute kidney injury and preventing subsequent renal fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.