ArticleCell death & disease2020
Involvement of FATP2-mediated tubular lipid metabolic reprogramming in renal fibrogenesis.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Lipid homeostasis in diabetic kidney disease.International journal of biological sciences · 2024Pooled it
- Fatty Kidney: The Interplay of Lipids and Diabetic Kidney Disease.Biomedicines · 2026Review
- Insulin Resistance and Inflammation.International journal of molecular sciences · 2026Review
- Fatty acid metabolism: opportunities and challenges of traditional Chinese medicine in the treatment of renal fibrosis.Chinese medicine · 2026Review
- Ectopic lipid deposition in kidney diseases: mechanisms in specific cell types and therapeutic strategies.Frontiers in endocrinology · 2026Review
- FATP2 at the crossroads of fatty acid transport, lipotoxicity, and complex disease.The Journal of clinical investigation · 2025Article
- Article
- Altered behaviour and immune response in mice with NHLRC2 p.Asp148Tyr variant.Brain, behavior, & immunity - health · 2025Article
- Pathogenesis and Therapeutic Perspectives of Tubular Injury in Diabetic Kidney Disease: An Update.Biomedicines · 2025Review
- SLC27A2 marks lipid peroxidation in nasal epithelial cells driven by type 2 inflammation in chronic rhinosinusitis with nasal polyps.Experimental & molecular medicine · 2025Article
- Crosstalk between glomeruli and tubules.Nature reviews. Nephrology · 2025Review
- ATGL regulates renal fibrosis by reprogramming lipid metabolism during the transition from AKI to CKD.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- ACOT12, a novel factor in the pathogenesis of kidney fibrosis, modulates ACBD5.Experimental & molecular medicine · 2025Article
- Metabolism at the crossroads of inflammation and fibrosis in chronic kidney disease.Nature reviews. Nephrology · 2025Review
- CEACAM6 facilitates gastric cancer progression through upregulating SLC27A2.Cancer gene therapy · 2025Article
- Identification of key lipid metabolism-related genes in kidney fibrosis: implications for chronic kidney disease management.Frontiers in physiology · 2025Article
- Targeting lipid metabolic reprogramming to alleviate diabetic kidney disease: molecular insights and therapeutic strategies.Frontiers in immunology · 2025Review
- Deciphering the Role of CD36 in Gestational Diabetes Mellitus: Linking Fatty Acid Metabolism and Inflammation in Disease Pathogenesis.Journal of inflammation research · 2025Review
- Unraveling Ferroptosis: A New Frontier in Combating Renal Fibrosis and CKD Progression.Biology · 2024Review
- Renal tubular epithelial cell quality control mechanisms as therapeutic targets in renal fibrosis.Journal of pharmaceutical analysis · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following a chronic insult, renal tubular epithelial cells (TECs) contribute to the development of kidney fibrosis through dysregulated lipid metabolism that lead to lipid accumulation and lipotoxicity. Intracellular lipid metabolism is tightly controlled by fatty acids (FAs) uptake, oxidation, lipogenesis, and lipolysis. Although it is widely accepted that impaired fatty acids oxidation (FAO) play a crucial role in renal fibrosis progression, other lipid metabolic pathways, especially FAs uptake, has not been investigated in fibrotic kidney. In this study, we aim to explore the potential mechanically role of FAs transporter in the pathogenesis of renal fibrosis. In the present study, the unbiased gene expression studies showed that fatty acid transporter 2 (FATP2) was one of the predominant expressed FAs transport in TECs and its expression was tightly associated with the decline of renal function. Treatment of unilateral ureteral obstruction (UUO) kidneys and TGF-β induced TECs with FATP2 inhibitor (FATP2i) lipofermata restored the FAO activities and alleviated fibrotic responses both in vivo and in vitro. Moreover, the expression of profibrotic cytokines including TGF-β, connective tissue growth factor (CTGF), fibroblast growth factor (FGF), and platelet-derived growth factor subunit B (PDGFB) were all decreased in FATP2i-treated UUO kidneys. Mechanically, FATP2i can effectively attenuate cell apoptosis and endoplasmic reticulum (ER) stress induced by TGF-β treatment in cultured TECs. Taking together, these findings reveal that FATP2 elicits a profibrotic response to renal interstitial fibrosis by inducing lipid metabolic reprogramming including abnormal FAs uptake and defective FAO in TECs.
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