Evidence map›Paper›PMID 36797553›Full record

ReviewInternational urology and nephrology2023

The role of gut-dependent molecule trimethylamine N-oxide as a novel target for the treatment of chronic kidney disease.

Sai Pan, Delong Zhao, Shuwei Duan, Xiangmei Chen

Abstract readReview
PubMed Publisher
In one paragraph

Review in International urology and nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. The Gut-Kidney Axis in Chronic Kidney Diseases.Diagnostics (Basel, Switzerland) · 2024
    Review
  11. Review
  12. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Sai Pan *Medical College of the Chinese People's Liberation Army, Department of Nephrology, General Hospital of Chinese PLA, Institute of Nephrology of Chinese PLA, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, 28 Fuxing Road, Haidian District, Beijing, 100853, China.
Delong Zhao *Department of Nephrology, General Hospital of Chinese PLA, Institute of Nephrology of Chinese PLA, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, 28 Fuxing Road, Haidian District, Beijing, 100853, China.
Shuwei DuanDepartment of Nephrology, General Hospital of Chinese PLA, Institute of Nephrology of Chinese PLA, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, 28 Fuxing Road, Haidian District, Beijing, 100853, China.
Xiangmei ChenDepartment of Nephrology, General Hospital of Chinese PLA, Institute of Nephrology of Chinese PLA, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, 28 Fuxing Road, Haidian District, Beijing, 100853, China. xmchen301@126.com.
Chinese PLA General Hospital · CNState Key Laboratory of Kidney Diseases

Funding

Major Project of Beijing Municipal Science and Technology Commission D181100000118002Major Project of Beijing Municipal Science and Technology Commission D181100000118004National Key R&D Program 2018YFE0126600
6 · The paper itself

Abstract

Trimethylamine N-oxide (TMAO) is an intestinal uremic toxin molecule mainly excreted by the kidney. Therefore, the plasma TMAO concentration is significantly increased in chronic kidney disease (CKD) patients, and plasma TMAO can be cleared by dialysis. Furthermore, TMAO damage the kidney mainly through three mechanisms: oxidative stress, inflammation and endoplasmic reticulum stress. Clinical experiments have indicated that higher TMAO levels are strongly related to the elevated incidence and mortality of cardiovascular (CV) events in CKD patients. Moreover, experimental data have shown that high levels of TMAO directly aggravate atherosclerosis, thrombosis and enhance myocardial contractility, resulting in myocardial ischemia and stroke. Specially, there are currently four potential ways to reduce blood TMAO concentration or block the effect of TMAO, including reducing the intake of trimethylamine (TMA) precursors in the diet, regulating the intestinal flora to reduce TMA production, interrupting the role of flavin-dependent monooxygenase isoforms (FMOs) to reduce the generation of TMAO, and blocking the TMAO receptor protein kinase R-like endoplasmic reticulum kinase (PERK). We hope that more clinical studies and clinicians will focus on clinical treatment to reduce the concentration of TMAO and alleviate renal damage.

Indexed as

Gastrointestinal MicrobiomeRenal Insufficiency, ChronicHumansKidneyMethylaminesMethylaminestrimethyloxamineCKDGut microbiotaKidney injuryTMAOUremic toxin

Identifiers

PMID36797553
OpenAlexW4321055750

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.