Evidence map›Paper›PMID 33062239›Full record

ArticleTherapeutic advances in chronic disease2020

Poricoic acid A as a modulator of TPH-1 expression inhibits renal fibrosis

Dan-Qian Chen, Xia-Qing Wu, Lin Chen, He-He Hu, Yan-Ni Wang, Ying-Yong Zhao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Therapeutic advances in chronic disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  5. Poricoic Acid A attenuated TGF-β1-induced epithelial-mesenchymal transition in renal tubular epithelial cells through SPRY2/ERK signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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  12. Poricoic acid A attenuates renal fibrosis by inhibiting endoplasmic reticulum stress-mediated apoptosis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
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  16. The Role of Histone Deacetylases in Acute Lung Injury-Friend or Foe.International journal of molecular sciences · 2023
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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

6 authors at 2 institutions in 1 country.

Dan-Qian ChenFaculty of Life Science and Medicine, Northwest University, Xi'an, Shaanxi, China.
Xia-Qing WuFaculty of Life Science and Medicine, Northwest University, Xi'an, Shaanxi, China.
Lin ChenFaculty of Life Science and Medicine, Northwest University, Xi'an, Shaanxi, China.
He-He HuFaculty of Life Science and Medicine, Northwest University, Xi'an, Shaanxi, China.
Yan-Ni WangFaculty of Life Science and Medicine, Northwest University, Xi'an, Shaanxi, China.
Ying-Yong ZhaoFaculty of Life Science and Medicine, Northwest University, No. 229 Taibai North Road, Xi'an, Shaanxi 710069, China.ORCID https://orcid.org/0000-0002-0239-7342
Northwest University · CNChina-Japan Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRenal fibrosis is the common feature of chronic kidney disease (CKD). However, few drugs specifically target fibrogenesis due to the lack of an effective therapeutic target. Hence, it is urgent to find a therapeutic strategy that inhibits renal fibrosis. Here, we identified that poricoic acid A (PAA) as the modulator of tryptophan hydroxylase-1 (TPH-1), the key enzyme in tryptophan metabolism, exerted potent anti-fibrotic effects in the kidney.

methodsLentiviral vector, luciferase reporter activity assay and co-immunoprecipitation were used. The animal model of unilateral ureteral obstruction and adenine-induced chronic renal failure as well as transforming growth factor (TGF)-β1-treated epithelial cells NRK-52E and fibroblasts NRK-49F were used.

resultsTPH-1 was gradually decreased during CKD progression, while PAA treatment significantly increased TPH-1 expression to suppress renal fibrosis. Pharmacological overexpression of TPH-1 by PAA treatment exhibited anti-fibrosis and was linked to Wnt/β-catenin signaling activity. TPH-1 exhibited anti-fibrotic effects by suppressing epithelial cell injury and fibroblast activation, and PAA promoted TPH-1 expression and then suppressed the Wnt/β-catenin signaling pathway

conclusionPAA as a modulator of TPH-1 expression attenuated renal fibrosis through regulating the Wnt/β-catenin signaling pathway by acting on the protein stability of β-catenin and β-catenin-mediated transcription. TPH-1 was required for PAA to exert anti-fibrosis.

Indexed as

chronic kidney diseasefibroblastporicoic acid Arenal fibrosisTPH-1Wnt/β-catenin

Identifiers

PMID33062239
PMCPMC7534062
OpenAlexW3090036544

What OpenQuestion 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 OpenQuestion graph.