Evidence map›Paper›PMID 35355864›Full record

ArticleOxidative medicine and cellular longevity2022

Fluorofenidone Inhibits UUO/IRI-Induced Renal Fibrosis by Reducing Mitochondrial Damage.

Xiaohua Liao, Xin Lv, Yan Zhang, Yuanyuan Han, Jiajia Li, Jianhua Zeng, Damu Tang, Jie Meng, Xiangning Yuan, Zhangzhe Peng and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

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  4. The Role of Sirt3 in Kidney Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2025
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  15. Review
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  17. Article
  18. Article
  19. Review
  20. Roles of Mitochondrial DNA Damage in Kidney Diseases: A New Biomarker.International journal of molecular sciences · 2022
    Review
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

12 authors at 2 institutions in 2 countries.

Xiaohua LiaoDepartment of Nephrology, Xiangya Hospital, Central South University, Changsha Hunan, China.ORCID https://orcid.org/0000-0002-5425-604X
Xin LvDepartment of Nephrology, Xiangya Hospital, Central South University, Changsha Hunan, China.
Yan ZhangDepartment of Nephrology, Xiangya Hospital, Central South University, Changsha Hunan, China.
Yuanyuan HanDepartment of Nephrology, Xiangya Hospital, Central South University, Changsha Hunan, China.
Jiajia LiDepartment of Nephrology, Xiangya Hospital, Central South University, Changsha Hunan, China.
Jianhua ZengDepartment of Nephrology, Xiangya Hospital, Central South University, Changsha Hunan, China.
Damu TangHamilton Urologic Oncology Research Center (HUORC), St. Joseph's Hospital and Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Jie MengHunan Key Lab of Organ Fibrosis, Changsha Hunan, China.
Xiangning YuanDepartment of Nephrology, Xiangya Hospital, Central South University, Changsha Hunan, China.
Zhangzhe PengDepartment of Nephrology, Xiangya Hospital, Central South University, Changsha Hunan, China.
Lijian TaoDepartment of Nephrology, Xiangya Hospital, Central South University, Changsha Hunan, China.
Yanyun XieDepartment of Nephrology, Xiangya Hospital, Central South University, Changsha Hunan, China.ORCID https://orcid.org/0000-0002-2985-6414
Central South University · CNSt. Joseph’s Healthcare Hamilton · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Mitochondrial damage contributes to extracellular matrix (ECM) deposition and renal fibrosis. In this study, we aimed (1) to investigate whether fluorofenidone (AKF-PD) can attenuate mitochondrial damage in two renal fibrosis models: unilateral ureteral obstruction (UUO) and renal ischemia-reperfusion injury (IRI), and (2) to explore the underlying mechanism. Method: Mitochondrial damage and renal lesions were analyzed in the UUO and IRI models. Mitochondrial energy metabolism, mitochondrial biogenesis, and oxidative stress were measured to assess the effect of AKF-PD on mitochondrial damage and to explore the underlying mechanism. In addition, HK-2 cells were stimulated with TGF- Results: In both UUO and IRI models, AKF-PD relieved renal fibrosis, maintained mitochondrial structure, and increased mitochondrial DNA copy numbers. The protection was associated with (1) sustaining mitochondrial energy metabolism, evident by elevations of tricarboxylic acid (TCA) cycle enzymes and mitochondrial respiratory chain complexes; (2) improving mitochondrial biogenesis with increases of TFAM, NRF1, PGC-1 Conclusion: We demonstrate that AKF-PD inhibited renal fibrosis at least in part via protecting mitochondria from damages developed in the UUO and IRI models. The mitochondrial protection was associated with sustaining mitochondrial energy metabolism, improving mitochondrial biogenesis, and reducing mitochondrial oxidative stress. This research verified the protective effect of AKF-PD on mitochondria in the UUO and IRI models and elaborated the underlying mechanism.

Indexed as

Kidney DiseasesUreteral ObstructionFibrosisHumansPyridones5-methyl-1-(3-fluorophenyl)-2-(1H)-pyridonePyridones

Identifiers

PMID35355864
PMCPMC8958071
OpenAlexW4221125792

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.