Evidence map›Paper›PMID 33504771›Full record

ArticleCell death & disease2021

P2X7 receptor signaling promotes inflammation in renal parenchymal cells suffering from ischemia-reperfusion injury.

Yingying Qian, Cheng Qian, Kewei Xie, Qicheng Fan, Yucheng Yan, Renhua Lu, Lin Wang, Minfang Zhang, Qin Wang, Shan Mou and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. [Electroacupuncture Alleviates Acute Kidney Injury in Septic Mice By Inhibiting the P2RX7/NLRP3 Signaling Pathway].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
    Article
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  9. Article
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  11. Review
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  14. Review
  15. Role of G protein coupled receptors in acute kidney injury.Cell communication and signaling : CCS · 2024
    Review
  16. Review
  17. Review
  18. 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

14 authors at 3 institutions in 1 country.

Yingying Qian *Department of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Cheng Qian *Department of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Kewei Xie *Department of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Qicheng FanDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Yucheng YanDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Renhua LuDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Lin WangDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Minfang ZhangDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Qin WangDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Shan MouDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Huili DaiDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Zhaohui NiDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Huihua PangDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Leyi GuDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. guleyi@aliyun.com.
Shanghai Jiao Tong University · CNRenji Hospital · CNHangzhou First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular adenosine triphosphate (ATP) and its receptor, P2X7 receptor (P2X7R), are playing an important role in the pathological process of renal ischemia-reperfusion injury, but their underlying mechanism remains unclear. Also, the effects of tubular epithelium-expressed P2X7 receptor on ischemia acute kidney injury is still unknown. The aim of this study is to clarify if this mechanism involves the activation of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome in the renal tubular epithelial cells. In our research, we used male C57BL/6 wild type and P2X7R (-/-) mice, cultured human proximal tubular epithelial cells, and kidneys from acute kidney injury patients. Mice underwent for unilateral nephrectomy combined with the lateral renal pedicle clamping. Cultured cells were subjected to hypoxia/reoxygenation or ATP. Apyrase and A438079 were used to block the extracellular ATP/P2X7 receptor pathway. We also constructed radiation-induced bone marrow (BM) chimeras by using P2X7R (-/-) mice and P2X7R (+/+) wild-type mice. P2X7 receptor deficiency protected from renal ischemia-reperfusion injury and attenuated the formation of NLRP3 inflammasome. By using BM chimeras, we found a partial reduction of serum creatinine and less histological impairment in group wild-type BM to P2X7R (-/-) recipient, compared with group wild-type BM to wild-type recipient. In renal tubular epithelial cells, hypoxia/reoxygenation induced ATP release and extracellular ATP depletion reduced the expression of active IL-1β. ATP activated the NLRP3 inflammasome in renal tubular epithelial cells, which were blunted by transient silence of P2X7 receptor, as well as by P2X7 receptor blocking with A438079. In human samples, we found that patients with Stage 3 AKI had higher levels of P2X7 receptor expression than patients with Stage 1 or Stage 2. Extracellular ATP/P2X7 receptor axis blocking may protect renal tubular epithelial cells from ischemia-reperfusion injury through the regulation of NLRP3 inflammasome.

Indexed as

Acute Kidney InjuryAnimalsFemaleHumansInflammationMaleMiceReceptors, Purinergic P2X7Reperfusion InjurySignal TransductionSurvival AnalysisTransfectionP2RX7 protein, humanP2rx7 protein, mouseReceptors, Purinergic P2X7

Identifiers

PMID33504771
PMCPMC7841183
OpenAlexW3125528918

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.