ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025
Podocyte FFAR4 deficiency aggravated glomerular diseases and aging.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Targeting LRH-1 alleviates diabetes-induced lipotoxicity in podocytes: role of PLIN5-mediated lipid droplet turnover.Renal failure · 2026Article
- Mentha-mediated selenium nanoparticles attenuate adriamycin-induced chronic kidney disease via multi-target modulation of oxidative, inflammatory, and fibrotic pathways.Biomaterials and biosystems · 2026Article
- New insights into diagnostic values and mechanisms of ferroptosis associated with immune infiltration in diabetic kidney disease.Experimental and therapeutic medicine · 2026Article
- S100A1 Promotes MDM2-Mediated KLF15 Ubiquitination to Regulate ID1-Driven Tubular Injury in Diabetic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- FFAR4 Mediates High-Altitude Hypoxia-Induced Asthenozoospermia through Oxidative Stress and Mitochondrial Dysfunction: An Integrative Bioinformatics and Experimental Study.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Tubular Omega-3 Fatty Acid Receptor FFAR4 Deficiency Aggravated Renal Aging and Chronic Kidney Disease.Aging cell · 2026Article
- FFAR4 negatively regulates colorectal cancer growth via blocking oxidative phosphorylation.Journal of translational medicine · 2026Article
- From a Shared Stress to Cell-Type-Specific Responses: The Heterogeneous Mechanisms of High Glucose-Induced Cellular Senescence in Diabetic Kidney Disease.Journal of diabetes research · 2026Review
- Lipid metabolism drives podocyte injury in diabetic kidney disease.Frontiers in immunology · 2026Review
- Review
- Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications.International journal of biological sciences · 2025Review
- The Lipid-Oxidative Stress Axis: Novel Therapeutic Targets for Podocytopathy.Journal of inflammation research · 2025Review
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Authors and funding
13 authors.
Funding
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Abstract
Podocyte injury contributes to the progression of glomerular disease and aging; however, causative molecular/physiological pathways are poorly defined, and there are few therapies to improve kidney outcomes. We previously reported that free fatty acid receptor 4 (FFAR4) agonist TUG891 improved podocyte injury to alleviate renal inflammation and fibrosis in diabetic nephropathy. However, the role of podocyte FFAR4 as a promising drug target has not been explored in glomerular diseases and aging. Here, we found that glomerular FFAR4 expression was abnormally decreased in patients and highly correlated with kidney function decline of glomerular diseases. Similarly, podocyte FFAR4 decreased in experimental focal segmental glomerulosclerosis and diabetic kidney disease mice. Both systemic and podocyte-specific FFAR4 deletion aggravated glomerular damage, whereas administration of FFAR4 agonist TUG891 and fish oil alleviated the severity of disease in adriamycin-induced nephropathy, diabetic, and aging mice, respectively. Mechanistically, FFAR4 reduction triggered cellular senescence and lipid metabolism disorder in injured podocytes and glomerulus. FFAR4 agonism exerted anti-senescent and anti-lipotoxic effects via activating CaMKKβ-AMPK signaling to protect against podocyte damage. These findings provide insight into signaling pathways involved in podocyte injury and enhance the understanding of the mechanistic functions of FFAR4 to reveal promising therapeutic opportunities against glomerular diseases and aging.
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