Evidence map›Paper›PMID 31257491›Full record

ArticleMolecular medicine reports2019

RIPK3 mediates renal tubular epithelial cell apoptosis in endotoxin‑induced acute kidney injury.

Shu Zhang, Ruizhao Li, Wei Dong, Huan Yang, Li Zhang, Yuanhan Chen, Weidong Wang, Chunling Li, Yanhua Wu, Zhiming Ye and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  7. Macrophage angiotensin ATAmerican journal of physiology. Renal physiology · 2023
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  9. Regulated cell death pathways in kidney disease.Nature reviews. Nephrology · 2023
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  14. miR-23a-3p inhibits sepsis-induced kidney epithelial cell injury by suppressing Wnt/β-catenin signaling by targeting wnt5a.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022
    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

15 authors at 4 institutions in 1 country.

Shu ZhangThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Ruizhao LiDivision of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Wei DongDivision of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Huan YangDivision of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Li ZhangDivision of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Yuanhan ChenDivision of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Weidong WangInstitute of Hypertension, Zhongshan School of Medicine, Sun Yat‑sen University, Guangzhou, Guangdong 510008, P.R. China.
Chunling LiInstitute of Hypertension, Zhongshan School of Medicine, Sun Yat‑sen University, Guangzhou, Guangdong 510008, P.R. China.
Yanhua WuDivision of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Zhiming YeDivision of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Xingchen ZhaoDivision of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Zhilian LiDivision of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Mengxi ZhangThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Shuangxin LiuDivision of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.
Xinling LiangThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Guangdong Provincial People's Hospital · CNGuangdong Academy of Medical Sciences · CNSouthern Medical University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal tubular epithelial cell apoptosis is an important pathological mechanism of septic acute kidney injury (AKI). Endotoxin, also known as lipopolysaccharide (LPS), has a key role in septic AKI and can directly induce tubular epithelial cell apoptosis. The upregulation of receptor‑interacting protein kinase 3 (RIPK3) in tubular epithelial cells has been reported in septic AKI, with RIPK3 mediating apoptosis in several cell types. In the present study, the effect of RIPK3 on endotoxin‑induced AKI was investigated in mouse tubular epithelial cell apoptosis in vitro and in vivo. It was found that the expression of RIPK3 was markedly increased in endotoxin‑induced AKI. Endotoxin‑induced AKI and tubular epithelial cell apoptosis could be attenuated by GSK'872, a RIPK3 inhibitor. LPS stimulation also upregulated RIPK3 expression in tubular epithelial cells in a time‑dependent manner. Both RIPK3 inhibitor and small interfering RNA (siRNA) targeting RIPK3 reduced LPS‑induced tubular epithelial cell apoptosis in vitro. The expression of the proapoptotic protein Bax was induced by LPS and reversed by GSK'872 or RIPK3‑siRNA. The present study revealed that RIPK3 mediated renal tubular cell apoptosis in endotoxin‑induced AKI. RIPK3 may be a potential target for the prevention of renal tubular cell apoptosis in endotoxin‑induced AKI.

Indexed as

Acute Kidney InjuryAnimalsApoptosisCells, CulturedDisease Models, AnimalEndotoxinsEpithelial CellsKidney TubulesMaleMice, Inbred C57BLReceptor-Interacting Protein Serine-Threonine KinasesEndotoxinsReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouse

Identifiers

PMID31257491
PMCPMC6625383
OpenAlexW2955783488

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.