Evidence map›Paper›PMID 34013370›Full record

ArticleMolecular medicine reports2021

Hydrogen sulfide attenuates renal I/R‑induced activation of the inflammatory response and apoptosis via regulating Nrf2‑mediated NLRP3 signaling pathway inhibition.

Yonghong Su, Yaoqi Wang, Min Liu, Hongguang Chen

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. 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
3.3field-weighted citation impact, top 7% 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, 30 citations in OpenAlex.

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  10. Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024
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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

4 authors at 2 institutions in 1 country.

Yonghong Su *Department of Pediatric Surgery, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China.
Yaoqi Wang *Department of Anesthesiology, Tianjin Medical University General Hospital, Cangzhou, Hebei 061001, P.R. China.
Min LiuDepartment of Urinary Surgery, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China.
Hongguang ChenDepartment of Anesthesiology, Tianjin Medical University General Hospital, Cangzhou, Hebei 061001, P.R. China.
Cangzhou Central Hospital · CNTianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal ischemia/reperfusion (I/R) injury can lead to acute renal failure, delayed graft function and graft rejection. Nucleotide‑binding oligomerization domain NOD‑like receptor containing pyrin domain 3 (NLRP3)‑mediated inflammation participates in the development of renal injury. Nrf2 accelerates NLRP3 signaling pathway activation and further regulates the inflammatory response. In addition, hydrogen sulfide serves a protective role in renal injury; however, the detailed underlying mechanism remains poorly understood. The present study investigated whether Nrf2 and NLRP3 pathway participate in hydrogen sulfide‑regulated renal I/R‑induced activation of the inflammatory response and apoptosis. Wild‑type and Nrf2‑knockout (KO) mice underwent surgery to induce renal I/R via clamping of the bilateral renal pedicles. A total of 20 mg/kg MCC950 (an NLRP3 inhibitor) was injected intraperitoneally daily for 14 days prior to surgery. Renal tissue and blood were collected from the I/R model mice to analyze NLRP3 and Nrf2 mRNA expression levels, NLRP3, PYD and CARD domain containing, caspase‑1, IL‑1β, Nrf2 and heme oxygenase 1 protein expression levels, cell apoptosis, the secretion of tumor necrosis factor‑α, IL‑1β and IL‑6 cytokines and renal histopathology and function. Renal I/R activated the NLRP3 and Nrf2 signaling pathways. Conversely, MCC950 treatment inhibited activation of the NLRP3 signaling pathway, and prevented I/R‑induced renal injury, release of cytokines and apoptosis in renal I/R model mice. Sodium hydrosulfide (NaHS) not only alleviated upregulation of NLRP3 protein expression levels, but also relieved renal injury, release of cytokines and cell apoptosis induced by renal I/R in wild‑type mice, but not in Nrf2‑KO mice. NaHS alleviated NLRP3 inflammasome activation, renal injury, the inflammatory response and cell apoptosis via the Nrf2 signaling pathway in renal I/R model mice.

Indexed as

Acute Kidney InjuryAnimalsApoptosisCaspase 1Gene Expression RegulationHeme Oxygenase-1Hydrogen SulfideInflammasomesInterleukin-1betaIschemiaKidneyMaleMiceMice, KnockoutNF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinCaspase 1Heme Oxygenase-1Hydrogen SulfideIL1B protein, mouseInflammasomesInterleukin-1betaNfe2l2 protein, mouseNF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseapoptosishydrogen sulfideNLR family pyrin domain containing 3Nrf2renal ischemia/reperfusion injury

Identifiers

PMID34013370
PMCPMC8160482
OpenAlexW3160620265

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.