ArticlePloS one2015
CD36 Mediated Fatty Acid-Induced Podocyte Apoptosis via Oxidative Stress.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 163 citations in OpenAlex.
- Kidney-Vascular Metabolic Crosstalk: Altered Lipoproteins in CKD.Circulation research · 2026Review
- Chaperone-mediated autophagy ameliorates hyperlipidemia-induced apoptosis in podocytes via attenuating lipid accumulation.Journal of molecular histology · 2026Article
- SSO targets CD36 to regulate lipid metabolism disorders and improve SiOCurrent research in toxicology · 2026Article
- The lipid-podocyte axis: emerging clues in membranous nephropathy pathogenesis.Frontiers in medicine · 2026Review
- Obesity and oxidative stress: potential mechanisms in endometrial disorders.Frontiers in endocrinology · 2026Review
- Regulation of lipoprotein processing by GPNMB in foamy macrophages: potential therapeutic targets for atherosclerosis.Nature communications · 2025Article
- Exploring the molecular mechanism of budesonide enteric capsules in the treatment of IgA nephropathy based on bioinformatics.Scientific reports · 2025Article
- Lipid Accumulation and Insulin Resistance: Bridging Metabolic Dysfunction-Associated Fatty Liver Disease and Chronic Kidney Disease.International journal of molecular sciences · 2025Review
- Human CD36: Gene Regulation, Protein Function, and Its Role in Atherosclerosis Pathogenesis.Genes · 2025Review
- Genotype-Based Molecular Mechanisms in Alport Syndrome.Journal of the American Society of Nephrology : JASN · 2025Review
- Integrating bioinformatics and machine learning to identify glomerular injury genes and predict drug targets in diabetic nephropathy.Scientific reports · 2025Article
- Review
- Protective effects of Notoginsenoside R2 on reducing lipid accumulation and mitochondrial dysfunction in diabetic nephropathy through regulation of c-Src.Chinese medicine · 2025Article
- Research progress in the treatment of lipid metabolism disorder in patients with diabetic kidney disease by the integrated traditional Chinese and Western medicine.Frontiers in endocrinology · 2025Review
- Article
- Multiple Roles of Palmitic Acid in Cardiovascular Diseases.Journal of inflammation research · 2025Review
- Identification and Validation of Aging-Related Genes in IgA Nephropathy in the Asian Population.International journal of general medicine · 2025Article
- From Adipose to Ailing Kidneys: The Role of Lipid Metabolism in Obesity-Related Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Bioinformatic analyses reveal lysosomal-associated protein transmembrane 5 as a potential therapeutic target in lipotoxicity-induced injury in diabetic kidney disease.Renal failure · 2024Article
- Does the Composition of Gut Microbiota Affect Chronic Kidney Disease? Molecular Mechanisms Contributed to Decreasing Glomerular Filtration Rate.International journal of molecular sciences · 2024Review
31 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHyperlipidemia-induced apoptosis mediated by fatty acid translocase CD36 is associated with increased uptake of ox-LDL or fatty acid in macrophages, hepatocytes and proximal tubular epithelial cells, leading to atherosclerosis, liver damage and fibrosis in obese patients, and diabetic nephropathy (DN), respectively. However, the specific role of CD36 in podocyte apoptosis in DN with hyperlipidemia remains poorly investigated.
methodsThe expression of CD36 was measured in paraffin-embedded kidney tissue samples (Ctr = 18, DN = 20) by immunohistochemistry and immunofluorescence staining. We cultured conditionally immortalized mouse podocytes (MPC5) and treated cells with palmitic acid, and measured CD36 expression by real-time PCR, Western blot analysis and immunofluorescence; lipid uptake by Oil red O staining and BODIPY staining; apoptosis by flow cytometry assay, TUNEL assay and Western blot analysis; and ROS production by DCFH-DA fluorescence staining. All statistical analyses were performed using SPSS 21.0 statistical software.
resultsCD36 expression was increased in kidney tissue from DN patients with hyperlipidemia. Palmitic acid upregulated CD36 expression and promoted its translocation from cytoplasm to plasma membrane in podocytes. Furthermore, palmitic acid increased lipid uptake, ROS production and apoptosis in podocytes, Sulfo-N-succinimidyloleate (SSO), the specific inhibitor of the fatty acid binding site on CD36, decreased palmitic acid-induced fatty acid accumulation, ROS production, and apoptosis in podocytes. Antioxidant 4-hydroxy-2,2,6,6- tetramethylpiperidine -1-oxyl (tempol) inhibited the overproduction of ROS and apoptosis in podocytes induced by palmitic acid.
conclusionsCD36 mediated fatty acid-induced podocyte apoptosis via oxidative stress might participate in the process of DN.
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