Evidence map›Paper›PMID 37706594›Full record

ArticleJournal of biochemical and molecular toxicology2023

Poricoic acid A induces mitophagy to ameliorate podocyte injury in diabetic kidney disease via downregulating FUNDC1.

Yuwen Wu, Haohua Deng, Jiazhong Sun, Jun Tang, Xin Li, Yancheng Xu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of biochemical and molecular toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

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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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  16. 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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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 1 institution in 1 country.

Yuwen WuDepartment of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.ORCID http://orcid.org/0009-0000-1398-502X
Haohua DengDepartment of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Jiazhong SunDepartment of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Jun TangDepartment of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Xin LiDepartment of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Yancheng XuDepartment of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.
Wuhan University · CN

Funding

Health Commission of Hubei Province Scientific Research Project WJ2021M161
6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is a devastating complication of diabetes mellitus (DM) and is the most prevalent chronic kidney disease (CKD). Poricoic acid A (PAA), a component isolated from Traditional Chinese Medicine (TCM) Poria cocos, has hypoglycaemic and anti-fibrosis effects. However, the role of PAA in DKD remains largely unclear. To mimics an in vitro model of DKD, the mouse podocyte MPC5 cells were treated with high glucose (25 mM; HG) for 24 h. CCK-8 and flow cytometry assays were conducted for assessing MPC5 cell viability and apoptosis. Meanwhile, streptozotocin (STZ) was used to induce experimental DKD in mice by intraperitoneal injection. PAA notably inhibited the apoptosis and inflammation, reduced the generation of ROS, and elevated the MMP level in HG-treated MPC5 cells. Moreover, PAA obviously reduced blood glucose and urine protein levels, inhibited renal fibrosis in DKD mice. Meanwhile, PAA markedly increased LC3 and ATG5 levels and declined p62 and FUNDC1 levels in HG-treated MPC5 cells and in the kidney tissues of DKD mice, leading to the activation of cell mitophagy. Furthermore, the downregulation of FUNDC1 also inhibited apoptosis, inflammation, and promoted mitophagy in HG-treated MPC5 cells. As expected, the knockdown of FUNDC1 further enhanced the protective role of PAA in MPC5 cells following HG treatment, indicating that induction of mitophagy could attenuate podocyte injury. Collectively, PAA could exert beneficial effects on podocyte injury in DKD by promoting mitophagy via downregulating FUNDC1. These findings suggested that PAA may have great potential in alleviating kidney injury in DKD.

Indexed as

Diabetes MellitusDiabetic NephropathiesPodocytesAnimalsInflammationMembrane ProteinsMiceMitochondrial ProteinsMitophagyTriterpenesFUNDC1 protein, mouseMembrane ProteinsMitochondrial Proteinsporicoic acid ATriterpenesdiabetes mellitusdiabetic kidney diseasemitophagypodocyteporicoic acid A

Identifiers

PMID37706594
PMCPMC13546950
OpenAlexW4386726062

What OpenQuestion holds

Textmetadata
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.