Evidence map›Paper›PMID 42244400›Full record

ArticleMediators of inflammation2026

Qingxin Lianzi Yin Improves Chronic Kidney Disease by Targeting Ferroptosis via the TLR4/HIF-1α Pathway.

Binqi Wang, Bo Lin, Danna Zheng, Luxi Cao

Abstract read
In one paragraph

Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Article
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.

Binqi WangDepartment of Nephrology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Urology and Nephrology Center, Hangzhou, Zhejiang, China, hospitalstar.com.ORCID https://orcid.org/0009-0006-3925-6953
Bo LinDepartment of Nephrology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Urology and Nephrology Center, Hangzhou, Zhejiang, China, hospitalstar.com.
Danna ZhengDepartment of Nephrology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Urology and Nephrology Center, Hangzhou, Zhejiang, China, hospitalstar.com.ORCID https://orcid.org/0000-0001-6415-8585
Luxi CaoDepartment of Nephrology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Urology and Nephrology Center, Hangzhou, Zhejiang, China, hospitalstar.com.ORCID https://orcid.org/0009-0005-5948-7372

Funding

Medical Science and Technology Project of Zhejiang Province 2023ZR063Medical Science and Technology Project of Zhejiang Province 2024ZL008
6 · The paper itself

Abstract

backgroundFerroptosis is involved in the pathogenesis of chronic kidney disease (CKD). Qingxin Lianzi Yin (QXLZY) has shown significant advantages in CKD treatment. This investigation intended to explore the impact of QXLZY on ferroptosis in CKD.

methodsThe anti-CKD effects of QXLZY were evaluated using the 5/6 nephrectomy-induced rat model and TGF-β1-stimulated HK-2 cells. Oxidative stress and ferroptosis levels were assessed using commercial kits and western blot. The mechanism of QXLZY in CKD treatment was predicted through network pharmacology. TLR4 and HIF-1α levels were detected by western blot. The role of ferroptosis in CKD treatment by QXLZY was explored using the ferroptosis inducer erastin. HK-2 cells overexpressing TLR4 were treated with the HIF-1α inhibitor LW6 to investigate the underlying mechanism. QXLZY components identified through network pharmacology as potentially interacting with TLR4 were validated.

resultsQXLZY effectively alleviated renal injury and inhibited fibrosis and inflammation in CKD models. Moreover, QXLZY markedly suppressed oxidative stress and ferroptosis. However, the anti-CKD effects of QXLZY were partially counteracted by erastin. TLR4 and HIF-1α were identified as potential targets through which QXLZY regulates ferroptosis in CKD. Their levels were notably increased in CKD models but were decreased after QXLZY treatment. Overexpression of TLR4 reversed the anti-CKD effects of QXLZY, and this phenomenon was altered by LW6. Lauric acid (LA) and caprylic acid (CA) were bioactive components within QXLZY regulating the TLR4/HIF-1α pathway in CKD.

conclusionQXLZY inhibits ferroptosis by downregulating the TLR4/HIF-1α pathway, thereby alleviating renal fibrosis and improving CKD, with LA and CA potentially playing significant roles.

Indexed as

Drugs, Chinese HerbalFerroptosisHypoxia-Inducible Factor 1, alpha SubunitRenal Insufficiency, ChronicToll-Like Receptor 4AnimalsCell LineHumansMaleOxidative StressRatsRats, Sprague-DawleySignal TransductionDrugs, Chinese HerbalHypoxia-Inducible Factor 1, alpha SubunitToll-Like Receptor 4chronic kidney diseaseferroptosisHIF-1α pathwayQingxin Lianzi YinTLR4

Identifiers

PMID42244400
PMCPMC13238268

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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.