Evidence map›Paper›PMID 34021126›Full record

ArticleCell death & disease2021

CD36 promotes NLRP3 inflammasome activation via the mtROS pathway in renal tubular epithelial cells of diabetic kidneys.

Yanjuan Hou, Qian Wang, Baosheng Han, Yiliang Chen, Xi Qiao, Lihua Wang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 113 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 1 pooled it
7.1field-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

113 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

  1. Pooled it
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  3. Disulfiram Attenuates Adenine-Induced Renal Fibrosis by Modulating Inflammatory and Immunometabolic Responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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53 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

6 authors at 3 institutions in 2 countries.

Yanjuan HouDepartment of Nephrology, Second Hospital, Shanxi Medical University, Taiyuan, China.ORCID http://orcid.org/0000-0002-5197-7394
Qian WangDepartment of Nephrology, Second Hospital, Shanxi Medical University, Taiyuan, China.
Baosheng HanDepartment of Cardiac Surgery, Shanxi Cardiovascular Hospital, Taiyuan, China.
Yiliang ChenBlood Research Institute, Blood Center of Wisconsin, Milwaukee, WI, USA.
Xi QiaoDepartment of Nephrology, Second Hospital, Shanxi Medical University, Taiyuan, China.
Lihua WangDepartment of Nephrology, Second Hospital, Shanxi Medical University, Taiyuan, China. lihuawang236@126.com.
Shanxi Medical University · CNMedical College of Wisconsin · USShanxi Cardiovascular Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tubulointerstitial inflammation plays a key role in the pathogenesis of diabetic nephropathy (DN). Interleukin-1β (IL-1β) is the key proinflammatory cytokine associated with tubulointerstitial inflammation. The NLRP3 inflammasome regulates IL-1β activation and secretion. Reactive oxygen species (ROS) represents the main mediator of NLRP3 inflammasome activation. We previously reported that CD36, a class B scavenger receptor, mediates ROS production in DN. Here, we determined whether CD36 is involved in NLRP3 inflammasome activation and explored the underlying mechanisms. We observed that high glucose induced-NLRP3 inflammasome activation mediate IL-1β secretion, caspase-1 activation, and apoptosis in HK-2 cells. In addition, the levels of CD36, NLRP3, and IL-1β expression (protein and mRNA) were all significantly increased under high glucose conditions. CD36 knockdown resulted in decreased NLRP3 activation and IL-1β secretion. CD36 knockdown or the addition of MitoTempo significantly inhibited ROS production in HK-2 cells. CD36 overexpression enhanced NLRP3 activation, which was reduced by MitoTempo. High glucose levels induced a change in the metabolism of HK-2 cells from fatty acid oxidation (FAO) to glycolysis, which promoted mitochondrial ROS (mtROS) production after 72 h. CD36 knockdown increased the level of AMP-activated protein kinase (AMPK) activity and mitochondrial FAO, which was accompanied by the inhibition of NLRP3 and IL-1β. The in vivo experimental results indicate that an inhibition of CD36 could protect diabetic db/db mice from tubulointerstitial inflammation and tubular epithelial cell apoptosis. CD36 mediates mtROS production and NLRP3 inflammasome activation in db/db mice. CD36 inhibition upregulated the level of FAO-related enzymes and AMPK activity in db/db mice. These results suggest that NLRP3 inflammasome activation is mediated by CD36 in renal tubular epithelial cells in DN, which suppresses mitochondrial FAO and stimulates mtROS production.

Indexed as

AnimalsCD36 AntigensCells, CulturedDiabetes Mellitus, ExperimentalDiabetic NephropathiesEpithelial CellsHumansInflammasomesInflammationKidney TubulesMaleMiceMice, Inbred C57BLMitochondriaNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesCD36 AntigensInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen Species

Identifiers

PMID34021126
PMCPMC8140121
OpenAlexW3160662701

What OpenQuestion holds

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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.