NLRP3 Inflammasome Inhibition Attenuates Diabetic Kidney Injury via the Suppression of Ferroptosis: Mechanistic Insights from In Vivo and In Vitro Models.

Zhili Tian, Qinghua Yin, Chenglong Zhou, Xiaochu Wu, Fei Liu, Jun Li

Abstract read

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Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Zhili TianThe Center of Gerontology and Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, China.ORCID 0000-0002-5684-4654

Qinghua YinDepartment of Nephrology, West China Hospital, Sichuan University, Chengdu 610041, China.

Chenglong ZhouThe Center of Gerontology and Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, China.

Xiaochu WuNational Clinical Research Center for Geriatrics (WCHSCU), West China Hospital, Sichuan University, Chengdu 610041, China.

Fei LiuDepartment of Nephrology, West China Hospital, Sichuan University, Chengdu 610041, China.

Jun LiThe Center of Gerontology and Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, China.

Funding

Science and Technology Department of Sichuan Province 2022YFS0297Science and Technology Department of Sichuan Province 2022YFS0326the International Visiting Program for Excellent Young Scholars of Sichuan University and the Foundation of the National Research Center of Geriatrics Y2018A32the National Key Technologies R&D Program of China 2022YFC3602303

6 · The paper itself

Abstract

Diabetic kidney disease (DKD) is a primary cause of end-stage renal disease (ESRD), and while ferroptosis is known to contribute to DKD pathogenesis, the regulatory role of the NLRP3 inflammasome in this process remains elusive. To address this research gap, we explored whether NLRP3 inhibition alleviates DKD by suppressing ferroptosis using streptozotocin-induced diabetic wild-type and NLRP3-knockout C57BL/6 mice, alongside high-glucose-cultured (30 mM) human renal tubular epithelial (HK-2) cells with or without siNLRP3 transfection. Inflammatory cytokines (IL-6, TNF-α, and IL-1β) were measured using an ELISA; oxidative stress markers (CSSG, MDA, GSH, and ROS) and the iron ion content via colorimetric assays; mitochondrial morphology by transmission electron microscopy (TEM); and ferroptosis-related proteins (ACSL4, COX2, and GPX4) through Western blotting. Our findings demonstrate that NLRP3-knockout diabetic mice displayed markedly reduced urinary albumin excretion and serum creatinine levels (

Indexed as

Diabetes Mellitus, ExperimentalDiabetic NephropathiesFerroptosisInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsCell LineCytokinesHumansMaleMiceMice, Inbred C57BLMice, KnockoutMitochondriaOxidative StressCytokinesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousediabetic kidney diseaseferroptosisinflammatory cytokinesNLRP3 inflammasomeoxidative stress

Identifiers

PMID42196240

DOI10.3390/ijms27104257

PMCPMC13207044

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.