ArticleInternational journal of biological sciences2025
APT1-derived depalmitoylation of CD36 alleviates diabetes-induced lipotoxicity in podocytes.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- ZDHHC9-Mediated Palmitoylation of ACSL4 Drives Ferroptosis in Diabetes Mellitus-Induced Erectile Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PLIN5 Protects Against Ang II-Induced Podocyte Lipotoxicity by Interacting With FKBP8 and Preserving Lipid Droplet-Mitochondria Contact.Cell proliferation · 2026Article
- Targeting posttranslational modifications of oxidative stress pathways for the treatment of diabetic nephropathy.Journal of pharmaceutical analysis · 2026Review
- Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application.MedComm · 2026Review
- Cluster of Differentiation 36-Mediated Inflammation and Lipid Metabolism in Cardiovascular Diseases: From Mechanisms to Novel Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Post-translational protein S-palmitoylation in renal tubular injury: mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Ectopic lipid deposition in kidney diseases: mechanisms in specific cell types and therapeutic strategies.Frontiers in endocrinology · 2026Review
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Authors and funding
7 authors.
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Abstract
Cluster of Differentiation 36 (CD36), also known as scavenger receptor B2, plays a critical role in controlling podocyte lipid metabolism, mediating the onset and progression of diabetic kidney disease (DKD). However, the post-translational regulation of CD36 and its exact role in lipid transport within podocytes remain unclear. In this study, we elucidate the mechanism by which acyl-protein thioesterase 1 (APT1) depalmitoylates CD36 in podocytes. We reveal that APT1 interacts with CD36 and reduces its palmitoylation at Cys466 specifically, thereby promoting its trafficking from the plasma membrane to lysosomes for degradation. Diabetes-induced downregulation of APT1 redirects palmitoylated CD36 into the recycling pathway. Consequently, enhanced lipid uptake in podocytes leads to lipotoxicity. Conversely, APT1 overexpression mitigates lipid accumulation by enhancing lysosomal degradation and reducing plasma membrane-associated CD36. Our findings indicate that diabetes-induced APT1 deficiency promotes palmitoylated CD36 enrichment on plasma membranes through decreased APT1 expression, driving lipid overload and podocyte injury.
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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 Socratic graph.