Evidence map›Paper›PMID 38907332›Full record

ArticleMicrobiome2024

Gut microbiota dysbiosis in hyperuricaemia promotes renal injury through the activation of NLRP3 inflammasome.

Xinghong Zhou, Shuai Ji, Liqian Chen, Xiaoyu Liu, Yijian Deng, Yanting You, Ming Wang, Qiuxing He, Baizhao Peng, Ying Yang and 5 more

Abstract read
In one paragraph

Article in Microbiome, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

58 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Marine drugs · 2026
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  17. Gut microbiota dysbiosis promotes chronic kidney disease-associated atrial fibrillation through activation of the NLRP3 inflammasome.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
    Article
  18. Review
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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

15 authors.

Xinghong Zhou *Zhujiang Hospital of Southern Medical University, Guangzhou, 510280, China.
Shuai Ji *School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Liqian Chen *School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Xiaoyu Liu *School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Yijian DengSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Yanting YouSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Ming WangZhujiang Hospital of Southern Medical University, Guangzhou, 510280, China.
Qiuxing HeDongguan Hospital of Guangzhou University of Chinese Medicine, Dongguan, 523000, China.
Baizhao PengSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Ying YangSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Xiaohu ChenSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Hiu Yee KwanSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Lin ZhouNanfang Hospital of Southern Medical University, Guangzhou, 510515, China. zlecho@163.com.
Jieyu ChenSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China. jieyu@smu.edu.cn.
Xiaoshan ZhaoZhujiang Hospital of Southern Medical University, Guangzhou, 510280, China. zhaoxs@smu.edu.cn.

Funding

Innovation Team and Talents Cultivation Program of National Administration of Traditional Chinese Medicine ZYYCXTD-C-202001Joint Funds of National Natural Science Foundation of China U22A20365Key Project of National Natural Science Foundation of China 81830117National Natural Science Foundation of China 82274499National Natural Science Foundation of China 82305130Natural Science Foundation of Guangdong Province, China 2022A1515110810Natural Science Foundation of Guangdong Province, China 2023A1515012429
6 · The paper itself

Abstract

backgroundThe prevalence of hyperuricaemia (HUA), a metabolic disorder characterized by elevated levels of uric acid, is on the rise and is frequently associated with renal injury. Gut microbiota and gut-derived uremic toxins are critical mediators in the gut-kidney axis that can cause damage to kidney function. Gut dysbiosis has been implicated in various kidney diseases. However, the role and underlying mechanism of the gut microbiota in HUA-induced renal injury remain unknown.

resultsA HUA rat model was first established by knocking out the uricase (UOX). HUA rats exhibited apparent renal dysfunction, renal tubular injury, fibrosis, NLRP3 inflammasome activation, and impaired intestinal barrier functions. Analysis of 16S rRNA sequencing and functional prediction data revealed an abnormal gut microbiota profile and activation of pathways associated with uremic toxin production. A metabolomic analysis showed evident accumulation of gut-derived uremic toxins in the kidneys of HUA rats. Furthermore, faecal microbiota transplantation (FMT) was performed to confirm the effects of HUA-induced gut dysbiosis on renal injury. Mice recolonized with HUA microbiota exhibited severe renal injury and impaired intestinal barrier functions following renal ischemia/reperfusion (I/R) surgery. Notably, in NLRP3-knockout (NLRP3

conclusionOur results demonstrate that HUA-induced gut dysbiosis contributes to the development of renal injury, possibly by promoting the production of gut-derived uremic toxins and subsequently activating the NLRP3 inflammasome. Our data suggest a potential therapeutic strategy for the treatment of renal diseases by targeting the gut microbiota and the NLRP3 inflammasome. Video Abstract.

Indexed as

DysbiosisGastrointestinal MicrobiomeHyperuricemiaInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsDisease Models, AnimalFecal Microbiota TransplantationKidneyMaleMiceMice, Inbred C57BLMice, KnockoutRatsRNA, Ribosomal, 16SUrate OxidaseInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseNlrp3 protein, ratRNA, Ribosomal, 16SUrate OxidaseGut-derived uremic toxinsGut-kidney axisHyperuricaemiaMicrobiotaNLRP3 inflammasomeRenal injury

Identifiers

PMID38907332
PMCPMC11191305

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Registered trials

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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.