Evidence map›Paper›PMID 33416097›Full record

ArticleInternational journal of molecular medicine2021

Formononetin protects against cisplatin‑induced acute kidney injury through activation of the PPARα/Nrf2/HO‑1/NQO1 pathway.

Yan Hao, Jie Miao, Wenjia Liu, Li Peng, Yue Chen, Qing Zhong

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  13. Ivacaftor attenuates gentamicin-induced ototoxicity through the CFTR-Nrf2-HO1/NQO1 pathway.Redox report : communications in free radical research · 2024
    Article
  14. Article
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  16. Review
  17. The Antioxidant Action ofMolecules (Basel, Switzerland) · 2024
    Review
  18. The effect ofTranslational andrology and urology · 2024
    Article
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Yan Hao *Department of Nephrology, Zigong First People's Hospital, Zigong, Sichuan 643000, P.R. China.
Jie Miao *Department of Imaging Medicine, Sichuan Vocational College of Health and Rehabilitation, Zigong, Sichuan 643000, P.R. China.
Wenjia LiuDepartment of Nephrology, Zigong First People's Hospital, Zigong, Sichuan 643000, P.R. China.
Li PengDepartment of Nephrology, Zigong First People's Hospital, Zigong, Sichuan 643000, P.R. China.
Yue ChenDepartment of Nephrology, Zigong First People's Hospital, Zigong, Sichuan 643000, P.R. China.
Qing ZhongDepartment of Nephrology, Zigong First People's Hospital, Zigong, Sichuan 643000, P.R. China.
Zigong First People's Hospital · CNSecond Affiliated Hospital of Chengdu University of Traditional Chinese · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) is characterized by an abrupt deterioration of renal function. Formononetin (FOR) protects against cisplatin (CIS)‑induced AKI, and it has various potential pharmacological and biological effects, including anti‑inflammatory, antioxidative and anti‑apoptotic effects. The current study investigated the role of FOR in CIS‑induced AKI. Rats were treated with CIS to establish an AKI model, followed by treatment with FOR. HK‑2 cells were treated with CIS, FOR, GW6471 [a peroxisome proliferator‑activated receptor α (PPARα) antagonist], eupatilin (a PPARα agonist) and nuclear factor erythroid 2‑related factor 2 (Nrf2) small interfering RNA (siNrf2), and cell proliferation and apoptosis were determined by MTT and flow cytometry assays. The mRNA and proteins levels of PPARα, Nrf2, heme oxygenase‑1 (HO‑1) and NAD(P)H quinone dehydrogenase 1 (NQO1) were measured by reverse transcription‑quantitative PCR and western blotting. The results demonstrated that FOR attenuated the histopathological changes, the levels of blood urea nitrogen, creatinine, TNF‑α and IL‑1β, and the MDA content and MPO activity, whereas it enhanced CAT activity in the AKI rat model. Furthermore, FOR and eupatilin promoted cell viability and CAT activity, and increased the levels of PPARα, Nrf2 and HO‑1 and NQO1, but suppressed apoptosis and MPO activity, and reduced the levels of MDA, TNF‑α and IL‑1β in CIS‑treated HK‑2 cells. Notably, the aforementioned effects were reversed by GW6471 treatment or siNrf2 transfection. In conclusion, FOR protects against CIS‑induced AKI via activation of the PPARα/Nrf2/HO‑1/NQO1 pathway.

Indexed as

Acute Kidney InjuryAnimalsCisplatinHeme Oxygenase (Decyclizing)IsoflavonesMaleNAD(P)H Dehydrogenase (Quinone)NF-E2-Related Factor 2PPAR alphaRatsRats, WistarSignal TransductionCisplatinformononetinHeme Oxygenase (Decyclizing)Hmox1 protein, ratIsoflavonesNAD(P)H Dehydrogenase (Quinone)Nfe2l2 protein, ratNF-E2-Related Factor 2NQO1 protein, ratPPAR alphaacute kidney injurycisplatinformononetinperoxisome proliferator-activated receptor α/nuclear factor erythroid 2-related factor 2/heme oxygenase‑1/NAD(P)H quinone dehydrogenase 1

Identifiers

PMID33416097
PMCPMC7797437
OpenAlexW3109207077

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.