ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Deficiency of Nuclear Receptor Coactivator 3 Aggravates Diabetic Kidney Disease by Impairing Podocyte Autophagy.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 14 citations in OpenAlex.
- NCOA1 Attenuates High Glucose-Induced Mesangial Matrix Expansion Through ITGA5 Inhibition.Current medical science · 2026Article
- ANGPTL4 Exacerbates Renal Injury in Diabetic Kidney Disease by Impairing Podocyte Lipophagy via Compromised Lysosomal Degradative Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Elucidating the therapeutic targets and multi-target mechanisms of salvianolic acid A for diabetic nephropathy.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Isoprenaline alleviates diabetic kidney disease via multi-target inhibition of the cGAS-STING pathway.Bioscience reports · 2026Article
- Roles of the peroxisome proliferator-activated receptors (PPARs) in the pathogenesis of diabetic kidney disease (DKD).Cell death discovery · 2026Review
- Mesenchymal Stem Cell-Derived Exosomes miR-143-3p Attenuates Diabetic Kidney Disease by Enhancing Podocyte Autophagy via Bcl-2/Beclin1 Pathway.Biomedicines · 2026Article
- Fyn Kinase: A Potential Target in Glucolipid Metabolism and Diabetes Mellitus.Current issues in molecular biology · 2025Review
- Nuclear receptors in health and disease: signaling pathways, biological functions and pharmaceutical interventions.Signal transduction and targeted therapy · 2025Review
- Emerging insights into the role of visceral adipose tissue in diabetic kidney disease.Frontiers in nutrition · 2025Review
- Bioinformatics-based analysis and experimental validation of PANoptosis-related biomarkers and immune infiltration in diabetic nephropathy.Frontiers in endocrinology · 2025Article
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- [Euonymus alatus delays progression of diabetic kidney disease in mice by regulating EGFR tyrosine kinase inhibitor resistance signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Deficiency of Nuclear Receptor Coactivator 3 Aggravates Diabetic Kidney Disease by Impairing Podocyte Autophagy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Authors and funding
11 authors at 3 institutions in 1 country.
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Abstract
Nuclear receptors (NRs) are important transcriptional factors that mediate autophagy, preventing podocyte injury and the progression of diabetic kidney disease (DKD). However, the role of nuclear receptor coactivators that are powerful enhancers for the transcriptional activity of NRs in DKD remains unclear. In this study, a significant decrease in Nuclear Receptor Coactivator 3 (NCOA3) is observed in injured podocytes caused by high glucose treatment. Additionally, NCOA3 overexpression counteracts podocyte damage by improving autophagy. Further, Src family member, Fyn is identified to be the target of NCOA3 that mediates the podocyte autophagy process. Mechanistically, NCOA3 regulates the transcription of Fyn in a nuclear receptor, PPAR-γ dependent way. Podocyte-specific NCOA3 knockout aggravates albuminuria, glomerular sclerosis, podocyte injury, and autophagy in DKD mice. However, the Fyn inhibitor, AZD0530, rescues podocyte injury of NCOA3 knockout DKD mice. Renal NCOA3 overexpression with lentivirus can ameliorate podocyte damage and improve podocyte autophagy in DKD mice. Taken together, the findings highlight a novel target, NCOA3, that protects podocytes from high glucose injury by maintaining autophagy.
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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.