Evidence map›Paper›PMID 41488368›Full record

ArticleiScience2025

Indole-3-propionic acid exacerbates cisplatin-induced chronic kidney disease through the AHR/NF-κB signaling pathway.

Qian Wang, Jie Chen, Huini Chen, Dongning Liang, Hong Zhou, Juanjuan Chen, Yuan Gui, Fang Yao, Yudan Chen, Xi Zeng and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Review
  2. 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

13 authors.

Qian WangDivision of Nephrology, Nanfang Hospital, Southern Medical University, State Key Laboratory of Prevention and Treatment of Multi-organ Injury, National Clinical Research Center for Kidney Disease, Guangdong Provincial Institute of Nephrology, Guangdong Provincial Key Laboratory of Renal Failure Research, Guangzhou 510515, China.
Jie ChenGuangzhou University of Traditional Chinese Medicine First Affiliated Hospital, Guangzhou 510405, China.
Huini ChenDivision of Nephrology, Nanfang Hospital, Southern Medical University, State Key Laboratory of Prevention and Treatment of Multi-organ Injury, National Clinical Research Center for Kidney Disease, Guangdong Provincial Institute of Nephrology, Guangdong Provincial Key Laboratory of Renal Failure Research, Guangzhou 510515, China.
Dongning LiangDivision of Nephrology, Nanfang Hospital, Southern Medical University, State Key Laboratory of Prevention and Treatment of Multi-organ Injury, National Clinical Research Center for Kidney Disease, Guangdong Provincial Institute of Nephrology, Guangdong Provincial Key Laboratory of Renal Failure Research, Guangzhou 510515, China.
Hong ZhouDivision of Nephrology, Nanfang Hospital, Southern Medical University, State Key Laboratory of Prevention and Treatment of Multi-organ Injury, National Clinical Research Center for Kidney Disease, Guangdong Provincial Institute of Nephrology, Guangdong Provincial Key Laboratory of Renal Failure Research, Guangzhou 510515, China.
Juanjuan ChenDivision of Nephrology, Nanfang Hospital, Southern Medical University, State Key Laboratory of Prevention and Treatment of Multi-organ Injury, National Clinical Research Center for Kidney Disease, Guangdong Provincial Institute of Nephrology, Guangdong Provincial Key Laboratory of Renal Failure Research, Guangzhou 510515, China.
Yuan GuiDivision of Nephrology, Department of Medicine, University of Connecticut School of Medicine, Farmington, CT 06030, USA.
Fang YaoMedical Research Center of Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Yudan ChenDivision of Nephrology, Nanfang Hospital, Southern Medical University, State Key Laboratory of Prevention and Treatment of Multi-organ Injury, National Clinical Research Center for Kidney Disease, Guangdong Provincial Institute of Nephrology, Guangdong Provincial Key Laboratory of Renal Failure Research, Guangzhou 510515, China.
Xi ZengDivision of Nephrology, Nanfang Hospital, Southern Medical University, State Key Laboratory of Prevention and Treatment of Multi-organ Injury, National Clinical Research Center for Kidney Disease, Guangdong Provincial Institute of Nephrology, Guangdong Provincial Key Laboratory of Renal Failure Research, Guangzhou 510515, China.
Yaxiang MaDivision of Nephrology, Nanfang Hospital, Southern Medical University, State Key Laboratory of Prevention and Treatment of Multi-organ Injury, National Clinical Research Center for Kidney Disease, Guangdong Provincial Institute of Nephrology, Guangdong Provincial Key Laboratory of Renal Failure Research, Guangzhou 510515, China.
Dong ZhouDivision of Nephrology, Department of Medicine, University of Connecticut School of Medicine, Farmington, CT 06030, USA.
Haiyan FuDivision of Nephrology, Nanfang Hospital, Southern Medical University, State Key Laboratory of Prevention and Treatment of Multi-organ Injury, National Clinical Research Center for Kidney Disease, Guangdong Provincial Institute of Nephrology, Guangdong Provincial Key Laboratory of Renal Failure Research, Guangzhou 510515, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin is a commonly used chemotherapy agent for treating various solid tumors, but its clinical application is limited by nephrotoxicity. While the potential for cisplatin to cause chronic kidney disease (CKD) following repeated administration has been underexplored, effective therapeutic strategies for cisplatin-induced CKD are lacking. We found that cisplatin-induced CKD is characterized by renal dysfunction and inflammation, along with intestinal barrier impairment. 16S rRNA and metabolomics revealed that cisplatin disrupts the gut microbiome and raises levels of tryptophan metabolites-indole-3-propionic acid (IPA). Notably, oral administration of IPA reproduced similar harmful effects in cisplatin-induced CKD. Integrated analyses of the microbiome, metabolomics, Raman spectroscopy, and DESI-MSI indicated that IPA supplementation exacerbates the production of uremic toxins linked to tryptophan metabolism and promotes the growth of pathogenic bacteria. Our findings demonstrates that IPA exacerbates renal inflammation and fibrosis by regulating AHR/NF-κB signaling pathways, altering intestinal microbiome composition, and disrupting tryptophan metabolism.

Indexed as

Cell biologyMolecular biologyPharmacology

Identifiers

PMID41488368
PMCPMC12757543

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.