Evidence map›Paper›PMID 39607209›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2024

Poricoic acid A attenuates renal fibrosis by inhibiting endoplasmic reticulum stress-mediated apoptosis.

Hui Zhao, Tian Liu, Chang-E Yang, Yue-Huan Hu, Yan Niu, Sheng-Ping Lei, Lin Chen, Ming-Xia Zhang

Abstract read
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Biodiversity and Natural Product Potential of Indonesian Actinomycetes.Journal of microbiology and biotechnology · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
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  8. Article
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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

8 authors.

Hui ZhaoClinical Experimental Center, Xi'an Engineering Technology Research Center for Cardiovascular Active Peptides, Northwest University Affiliated Xi'an International Medical Center Hospital, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0001-8837-9120
Tian LiuClinical Experimental Center, Xi'an Engineering Technology Research Center for Cardiovascular Active Peptides, Northwest University Affiliated Xi'an International Medical Center Hospital, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0002-1569-2084
Chang-E YangClinical Experimental Center, Xi'an Engineering Technology Research Center for Cardiovascular Active Peptides, Northwest University Affiliated Xi'an International Medical Center Hospital, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0003-1911-1093
Yue-Huan HuClinical Experimental Center, Xi'an Engineering Technology Research Center for Cardiovascular Active Peptides, Northwest University Affiliated Xi'an International Medical Center Hospital, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0009-0720-5504
Yan NiuClinical Experimental Center, Xi'an Engineering Technology Research Center for Cardiovascular Active Peptides, Northwest University Affiliated Xi'an International Medical Center Hospital, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0002-6777-1593
Sheng-Ping LeiClinical Experimental Center, Xi'an Engineering Technology Research Center for Cardiovascular Active Peptides, Northwest University Affiliated Xi'an International Medical Center Hospital, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0002-0410-4523
Lin ChenCollege of Biology, Pharmacy and Food Engineering, Shangluo University, Shangluo, Shaanxi, China.ORCID http://orcid.org/0000-0003-3399-8711
Ming-Xia ZhangClinical Experimental Center, Xi'an Engineering Technology Research Center for Cardiovascular Active Peptides, Northwest University Affiliated Xi'an International Medical Center Hospital, Xi'an, Shaanxi, China.ORCID http://orcid.org/0009-0008-9492-5296

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal fibrosis is a common manifestation in the progression of chronic kidney disease (CKD) to kidney failure. Currently, there is no available therapy to prevent the progression of renal fibrosis. Poricoic acid A (PAA) isolated from Poria cocos shows notable antifibrotic effects. However, its potential mechanism is still unclear. This study aimed to evaluate the effects and the potential mechanisms of PAA against renal fibrosis. A mouse model of renal fibrosis was established using unilateral ureteral obstruction (UUO). We showed that PAA administration significantly alleviated renal lesions and collagen deposition in UUO mice. Mice with UUO resulted in epithelial-to-mesenchymal transition (EMT) and the activation of endoplasmic reticulum stress (ERS) in the renal tissues, while PAA treatment significantly inhibited EMT and ERS activation. Additionally, PAA markedly alleviated ERS-mediated apoptosis in UUO mice. Molecular docking results indicated that PAA stably combined to GRP78 and ATF4. In conclusion, these results demonstrated that PAA possesses a significant bioactivity against renal fibrosis and its treatment mechanism might be the inhibition of ERS-mediated apoptosis.

Indexed as

ApoptosisDisease Models, AnimalEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressFibrosisAnimalsEpithelial-Mesenchymal TransitionKidneyKidney DiseasesMaleMiceMice, Inbred C57BLMolecular Docking SimulationUreteral ObstructionEndoplasmic Reticulum Chaperone BiPHspa5 protein, mouse

Identifiers

PMID39607209
PMCPMC11653467

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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.