ArticleKidney international2020
Sterol-O-acyltransferase-1 has a role in kidney disease associated with diabetes and Alport syndrome.
Article in Kidney international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Lipid homeostasis in diabetic kidney disease.International journal of biological sciences · 2024Pooled it
- Review
- Lipid Metabolism Reprogramming in the Aging Brain: Glial-Mediated Pathogenic Mechanisms and Translational Strategies in Neurodegeneration.International journal of molecular sciences · 2026Review
- Organelle Crosstalk in Renal Cells: Insights from Cell Biology and Implications for AKI-to-CKD Transition.International journal of molecular sciences · 2026Review
- Lipid metabolic dysregulation in diabetic kidney disease: mechanisms, cellular impact, and therapeutic strategies.Journal of clinical & translational endocrinology · 2026Review
- Lipids in kidney diseases: from systemic imbalance to intrarenal alterations of cellular lipid metabolism in rare and common kidney diseases.Journal of molecular medicine (Berlin, Germany) · 2026Review
- The lipid-podocyte axis: emerging clues in membranous nephropathy pathogenesis.Frontiers in medicine · 2026Review
- Endoplasmic reticulum-mediated organelle crosstalk in kidney disease.Nature reviews. Nephrology · 2025Review
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Lipidomics Unveils Critical Lipid Pathway Shifts in Alport Syndrome.Kidney international reports · 2025Article
- Multiplatform Metabolomic Profiling of the Unilateral Ureteral Obstruction Murine Model of CKD.International journal of molecular sciences · 2025Article
- High-fat diet promotes lipotoxicity in the podocytes of uninephrectomized mice: a targeted lipidomics and kidney podocyte-specific analysis.Cell death discovery · 2025Article
- Enhancement of Intracellular Cholesterol Efflux in Chondrocytes Leading to Alleviation of Osteoarthritis Progression.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications.International journal of biological sciences · 2025Review
- Metabolism at the crossroads of inflammation and fibrosis in chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Asprosin Levels in Adults with Type 2 Diabetes Mellitus and Diabetic Kidney Disease: A Systematic Review and Meta-Analysis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Targeting lipid metabolic reprogramming to alleviate diabetic kidney disease: molecular insights and therapeutic strategies.Frontiers in immunology · 2025Review
- Mechanisms and implications of podocyte autophagy in chronic kidney disease.American journal of physiology. Renal physiology · 2024Review
- Molecular mechanism of renal lipid accumulation in diabetic kidney disease.Journal of cellular and molecular medicine · 2024Review
- The Role of Fatty Acid Synthase in the Vascular Smooth Muscle Cell to Foam Cell Transition.Cells · 2024Article
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17 authors at 2 institutions in 1 country.
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Abstract
Defective cholesterol metabolism primarily linked to reduced ATP-binding cassette transporter A1 (ABCA1) expression is closely associated with the pathogenesis and progression of kidney diseases, including diabetic kidney disease and Alport Syndrome. However, whether the accumulation of free or esterified cholesterol contributes to progression in kidney disease remains unclear. Here, we demonstrate that inhibition of sterol-O-acyltransferase-1 (SOAT1), the enzyme at the endoplasmic reticulum that converts free cholesterol to cholesterol esters, which are then stored in lipid droplets, effectively reduced cholesterol ester and lipid droplet formation in human podocytes. Furthermore, we found that inhibition of SOAT1 in podocytes reduced lipotoxicity-mediated podocyte injury in diabetic kidney disease and Alport Syndrome in association with increased ABCA1 expression and ABCA1-mediated cholesterol efflux. In vivo, Soat1 deficient mice did not develop albuminuria or mesangial expansion at 10-12 months of age. However, Soat1 deficiency/inhibition in experimental models of diabetic kidney disease and Alport Syndrome reduced cholesterol ester content in kidney cortices and protected from disease progression. Thus, targeting SOAT1-mediated cholesterol metabolism may represent a new therapeutic strategy to treat kidney disease in patients with diabetic kidney disease and Alport Syndrome, like that suggested for Alzheimer's disease and cancer treatments.
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Registered trials
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