Evidence map›Paper›PMID 32134954›Full record

ArticlePloS one2020

Angiotensin II triggers RIPK3-MLKL-mediated necroptosis by activating the Fas/FasL signaling pathway in renal tubular cells.

Yongjun Zhu, Hongwang Cui, Jie Lv, Guojun Li, Xiaoyan Li, Feng Ye, Liangbao Zhong

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Necroptosis in obesity: a complex cell death event.Apoptosis : an international journal on programmed cell death · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Targeting necroptosis in fibrosis.Molecular biology reports · 2023
    Review
  10. Article
  11. Review
  12. Role of the renin-angiotensin system in NETosis in the coronavirus disease 2019 (COVID-19).Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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

7 authors at 1 institution in 1 country.

Yongjun ZhuDepartment of Nephrology, the First Affiliated Hospital of Hainan Medical University, Haikou, China.ORCID 0000-0002-3630-3893
Hongwang CuiDepartment of Orthopedics, the First Affiliated Hospital of Hainan Medical University, Haikou, China.
Jie LvThe First Clinical College of Hainan Medical University, Hainan, China.
Guojun LiDepartment of Orthopedics, the First Affiliated Hospital of Hainan Medical University, Haikou, China.
Xiaoyan LiDepartment of Nephrology, the First Affiliated Hospital of Hainan Medical University, Haikou, China.
Feng YeDepartment of Nephrology, the First Affiliated Hospital of Hainan Medical University, Haikou, China.
Liangbao ZhongDepartment of Nephrology, the First Affiliated Hospital of Hainan Medical University, Haikou, China.
Hainan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our earlier studies proved that RIPK3-mediated necroptosis might be an important mode of renal tubular cell death in rats with chronic renal injury and the necroptotic cell death can be triggered by tumor necrosis factor-α (TNF-α) in vitro, but the triggering role of angiotensin II (AngII), which exerts notable effects on renal cells for the initiation and progression of renal tubulointerstitial fibrosis, is largely unknown. Here, we identified the presence of necroptotic cell death in the tubular cells of AngII-induced chronic renal injury and fibrosis mice and assessed the percentage of necroptotic renal tubular cell death with the disruption of this necroptosis by the addition of necrostatin-1 (Nec-1). Furthermore, the observation was further confirmed in HK-2 cells treated with AngII and RIPK1/3 or MLKL inhibitors. The detection of Fas and FasL proteins led us to investigate the contribution of the Fas/FasL signaling pathway to AngII-induced necroptosis. Disruption of FasL decreased the percentage of necroptotic cells, suggesting that Fas and FasL are likely key signal molecules in the necroptosis of HK-2 cells induced by AngII. Our data suggest that AngII exposure might trigger RIPK3-MLKL-mediated necroptosis in renal tubular epithelial cells by activating the Fas/FasL signaling pathway in vivo and in vitro.

Indexed as

Angiotensin IIAnimalsCell LineFas Ligand Proteinfas ReceptorFibrosisHumansKidney TubulesMaleMiceMice, Inbred C57BLNecroptosisProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionAngiotensin IIFas Ligand Proteinfas ReceptorMLKL protein, mouseProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouse

Identifiers

PMID32134954
PMCPMC7058379
OpenAlexW3010214713

What OpenQuestion holds

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LicenceCC BY
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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.