Evidence map›Paper›PMID 36620089›Full record

ReviewBiochemistry and biophysics reports2023

Chronic kidney disease and NLRP3 inflammasome: Pathogenesis, development and targeted therapeutic strategies.

Gengzhen Huang, Yaodan Zhang, Yingying Zhang, Yuerong Ma

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biochemistry and biophysics reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 2 pooled it
4.1field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.

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  5. NLRP3 Inflammasome Activation and Atherogenic Lipid Profile in Hemodialysis Patients.Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy · 2026
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2 more citing papers are in PubMed but not listed here.

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.

Gengzhen HuangChengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Yaodan ZhangHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, China.
Yingying ZhangChengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Yuerong MaChengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Chengdu University of Traditional Chinese Medicine · CNChengdu Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a global health concern and public health priority. The condition often involves inflammation due to the accumulation of toxins and the reduced clearance of inflammatory cytokines, leading to gradual loss of kidney function. Because of the tremendous burden of CKD, finding effective treatment strategies against inflammation is crucial. Substantial evidence suggests an association between kidney disease and the inflammasome. As a well-known multiprotein signaling complex, the NLR family pyrin domain containing 3 (NLRP3) inflammasome plays an important role in inducing renal inflammation and fibrosis. Small molecule inhibitors targeting the NLRP3 inflammasome are potential agents for the treatment of CKD.The NLRP3 inflammasome activation amplifies the inflammation response, promoting pyroptotic cell death. Thus, it may contribute to the onset and progression of CKD, but the mechanism behind inflammasome activation in CKD remains obscure.In this review, we summarized recent findings on the role of the NLRP3 inflammasome in CKD and new strategies targeting the NLRP3 inflammasome.

Indexed as

Ang II, Angiotensin IIASC, apoptosis-associated speck-like proteinChronic kidney diseaseCKD, Chronic kidney diseaseDAMPs, damage-associated molecular patternsESRD, End-stage renal diseaseGFR, glomerular filtration rateHK-2, renal tubular epithelial cells,IL-18, Interleukin-18IL-1β, Interleukin-1βInflammasomeKidney functionLRR, leucine-rich repeatNEK7, NIMA-related kinase 7NF-kB, nuclear factor kappa-BNLRP3, NLR family pyrin domain containing 3NOD-like receptorPAMPs, Pathogen-associated molecular patternsROS, reactive oxygen speciesTXNIP, thioredoxin-interacting protein

Identifiers

PMID36620089
PMCPMC9813680
OpenAlexW4312222002

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.