ArticleCell death & disease2022
CD36 aggravates podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy in lupus nephritis.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 75 citations in OpenAlex.
- Finerenone attenuates chronic fibrotic remodeling during the AKI-CKD transition in an ischemia-reperfusion-induced acute kidney injury mouse model.Renal failure · 2026Article
- Advances in understanding the NLRP3 inflammasome‑mediated mechanisms and therapeutic targets in diabetic nephropathy (Review).International journal of molecular medicine · 2026Review
- The TRAF6-TXNIP-NLRP3 signaling axis regulates LPS-induced pyroptosis in glomerular podocytes.Journal of molecular histology · 2026Article
- Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026Review
- From damage signals to immune modulators: oxidized lipids in immunometabolic inflammation.Journal of lipid research · 2026Review
- PHLDB1 and WDFY4 as dual-state biomarkers in SLE pathogenesis and lupus nephritis prediction.BMC immunology · 2026Article
- Human umbilical cord mesenchymal stem cell-derived exosomes are associated with changes in renal injury markers, gut microbiota composition, and inflammatory signaling in IgA nephropathy.Frontiers in immunology · 2026Article
- GBP2 promotes podocyte pyroptosis and contributes to the pathogenesis of pediatric lupus nephritis.PloS one · 2026Article
- Deciphering the interplay between inflammation and dysregulated autophagy in lupus nephritis through network analysis and experimental validation.Frontiers in cell and developmental biology · 2026Article
- Retinoic acid receptor β deletion in podocytes causes kidney and liver dysfunction, modeling nephrotic syndrome.Journal of molecular endocrinology · 2026Article
- Structural dynamics, pathogenic mechanisms, and therapeutic targeting of the NLRP3 inflammasome in lupus nephritis.Frontiers in immunology · 2026Review
- Retinitis Pigmentosa-Associated Gene TRIM49 Regulates ULK1-Mediated Autophagy and Photoreceptor Phagocytosis by the Retinal Pigment Epithelium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- Targeting autophagy in autoimmune glomerular diseases.Journal of nephrology · 2025Review
- The intelligent podocyte: sensing and responding to a complex microenvironment.Nature reviews. Nephrology · 2025Review
- Bioinformatic analysis and experimental verification reveal expansion of monocyte subsets with an interferon signature in systemic lupus erythematosus patients.Arthritis research & therapy · 2025Article
- Review
- Gene Expression in Urinary Sediment Cells as an Indicator of the Contribution of Plasma Lipids to Diabetic Kidney Disease.Journal of diabetes research · 2025Article
- APT1-derived depalmitoylation of CD36 alleviates diabetes-induced lipotoxicity in podocytes.International journal of biological sciences · 2025Article
- Metabolism at the crossroads of inflammation and fibrosis in chronic kidney disease.Nature reviews. Nephrology · 2025Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A major cause of proteinuria in lupus nephritis (LN) is podocyte injury, and determining potential therapeutic targets to prevent podocyte injury is important from a clinical perspective in the treatment of LN. CD36 is involved in podocyte injury in several glomerulopathies and was reported to be a vital candidate gene in LN. Here, we determined the role of CD36 in the podocyte injury of LN and the underlying mechanisms. We observed that CD36 and NLRP3 (NLR family pyrin domain containing 3) were upregulated in the podocytes of lupus nephritis patients and MRL/lpr mice with renal impairment. In vitro, CD36, NLRP3 inflammasome, and autophagy were elevated accompanied with increased podocyte injury stimulated by IgG extracted from lupus nephritis patients compared that from healthy donors. Knocking out CD36 with the CRISPR/cas9 system decreased the NLRP3 inflammasome levels, increased the autophagy levels and alleviated podocyte injury. By enhancing autophagy, NLRP3 inflammasome was decreased and podocyte injury was alleviated. These results demonstrated that, in lupus nephritis, CD36 promoted podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy by enhancing which could decrease NLRP3 inflammasome and alleviate podocyte injury.
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