Evidence map›Paper›PMID 42030211›Full record

ArticleKidney & blood pressure research2026

TRPC6 Inhibition Attenuates Renal Tubulointerstitial Fibrosis via the Reactive Oxygen Species/TXNIP/NLRP3 Signaling Pathway.

Linting Wei, Chenkai Cui, Yan Li, Pengbo Ge, Ke Li, Haodong Wang, Weihao Zhao, Yinhong Wang, Jianpeng Zhang, Rongguo Fu

Abstract read
In one paragraph

Article in Kidney & blood pressure research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Linting WeiDepartment of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Chenkai CuiDepartment of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Yan LiDepartment of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Pengbo GeDepartment of General Surgery, The First Affiliated Hospital of Xi'an Medical University, Xi'an, China.
Ke LiDepartment of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Haodong WangDepartment of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Weihao ZhaoDepartment of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Yinhong WangDepartment of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Jianpeng ZhangDepartment of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Rongguo FuDepartment of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China, fu_rongguo@sina.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionChronic kidney disease is a worldwide public health issue primarily characterized by glomerulosclerosis and the renal tubulointerstitial fibrosis. Recent studies have shown that TRPC6 is essential in renal interstitial fibrosis, although the precise mechanisms involved are not yet fully understood.

methodsUUO model was established using C57BL/6 male mice in which HK-2 cells were stimulated with TGF-β1. H&E and Masson staining were used to observe pathological changes. IHC staining was also conducted to measure the α-SMA, fibronectin (Fn), TRPC6, reactive oxygen species (ROS), and NLRP3 expressions. Scanning electron microscopy was used to observe morphological changes in the tubular cell membrane, and flow cytometry was utilized to measure ROS levels. In addition, Western blotting was performed to detect Fn, α-SMA, TRPC6, TXNIP, NLRP3, and the downstream pyroptosis-related molecule levels.

resultsTRPC6 protein levels were enhanced in UUO mice and HK-2 cells upon TGF-β1 stimulation, which coincided with noticeable morphological changes associated with pyroptosis. Treatment with the TRPC6 inhibitor SAR7334 effectively reduced renal fibrosis markers and diminished levels of ROS, TXNIP, and proteins related to NLRP3-mediated pyroptosis (including NLRP3, cGSDMD, and IL-1β). Furthermore, application of the NLRP3 inhibitor MCC950 in HK-2 cells reinforced our findings, as it attenuated renal fibrosis-related proteins and counteracted the elevated levels of Fn, α-SMA, and NLRP3-mediated pyroptosis proteins observed in TGF-β1-stimulated HK-2 cells. Additionally, inhibiting TRPC6 appeared to dampen the activity of the ROS/TXNIP/NLRP3 pathway.

conclusionTRPC6 may represent a promising target for mitigating renal interstitial fibrosis, potentially through its effects on the ROS/TXNIP regulatory pathway involving NLRP3-mediated pyroptosis.

Indexed as

Carrier ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesTRPC6 Cation ChannelAnimalsCell LineFibrosisHumansKidney TubulesMaleMiceMice, Inbred C57BLSignal TransductionThioredoxinsCarrier ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReactive Oxygen SpeciesThioredoxinsTRPC6 Cation ChannelTrpc6 protein, mouseTxnip protein, mouseNLRP3PyroptosisRenal tubular epithelial cellRenal tubulointerstitial fibrosisTRPC6

Identifiers

PMID42030211
PMCPMC13345608

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.