ArticleSignal transduction and targeted therapy2022
FFAR4 improves the senescence of tubular epithelial cells by AMPK/SirT3 signaling in acute kidney injury.
Article in Signal transduction and targeted therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
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Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Efficacy of traditional Chinese medicineFrontiers in medicine · 2024Pooled it
- Metabolic memory in the kidney: how lactate and lactylation drive the path from acute injury to chronic disease.Renal failure · 2026Review
- Fibrinogen-like protein 2-complement C3 interaction exacerbates tubular inflammation in acute kidney injury by elevating complement C3a levels.Renal failure · 2026Article
- Macrophage programming in systemic sclerosis: Niches, networks, and translational horizons.Seminars in immunopathology · 2026Review
- Tubular ACSM3 controls fatty acid metabolism and safeguards against acute kidney injury in male mice.Nature communications · 2026Article
- Integrative gene target mapping, RNA sequencing, in silico molecular docking, ADMET profiling and molecular dynamics simulation study of marine derived molecules for type 1 diabetes mellitus.Molecular diversity · 2026Article
- GαNature communications · 2026Article
- Integrated Stress Response and Drug-Induced Acute Kidney Injury: Involvement of Activating ATF4-STAT1-GBP2 Signaling.Journal of the American Society of Nephrology : JASN · 2026Article
- NAT10 inhibition alleviates renal tubular epithelial cell senescence by impeding ac4C acetylation of PAPP-A mRNA in diabetic nephropathy.Cell death & disease · 2026Article
- Tubular Omega-3 Fatty Acid Receptor FFAR4 Deficiency Aggravated Renal Aging and Chronic Kidney Disease.Aging cell · 2026Article
- UBC9-mediated p53 SUMOylation drives tubular senescence and exacerbates acute kidney injury in mice.Acta pharmacologica Sinica · 2026Article
- Dual Roles and Therapeutic Prospects of Proximal Tubular Epithelial Cell Senescence in Acute Kidney Injury.Biomolecules · 2026Review
- PARP7 alleviates lipopolysaccharide-induced acute kidney injury by inhibiting TBK1-driven inflammation in renal tubular epithelial cells.Molecular medicine (Cambridge, Mass.) · 2026Article
- Hypoxia-Inducible Factor-1α Drives Cellular Senescence via Autophagy Activation to Promote Acute Kidney Injury-to-CKD Transition.American journal of nephrology · 2026Article
- Endothelial Ffar4 protects against diabetic kidney disease by potentiating endogenous retinoic acid metabolism.Cellular & molecular biology letters · 2026Article
- SIRT3 attenuates AGEs-induced senescence in human granulosa cells through enhancing mitophagy.Cell biology and toxicology · 2026Article
- Elimination of Senescent Macrophages by Purinergic Receptor P2RX7 Antagonist to Safeguard Against Kidney Injury and Aging.International journal of biological sciences · 2026Article
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- CBX8 suppresses autophagy-dependent senescence in colorectal cancer by modulating the mTOR signaling pathway.International journal of biological sciences · 2026Article
- NAT10 Promotes Tubular Epithelial Cell Senescence in Cisplatin-Induced Acute Kidney Injury by Regulating DDX17.International journal of biological sciences · 2026Article
10 more citing papers are in PubMed but not listed here.
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10 authors at 1 institution in 1 country.
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Abstract
Acute kidney injury (AKI) is a serious clinical complication with high morbidity and mortality rates. Despite substantial progress in understanding the mechanism of AKI, no effective therapy is available for treatment or prevention. We previously found that G protein-coupled receptor (GPCR) family member free fatty acid receptor 4 (FFAR4) agonist TUG891 alleviated kidney dysfunction and tubular injury in AKI mice. However, the versatile role of FFAR4 in kidney has not been well characterized. In the study, the expression of FFAR4 was abnormally decreased in tubular epithelial cells (TECs) of cisplatin, cecal ligation/perforation and ischemia/reperfusion injury-induced AKI mice, respectively. Systemic and conditional TEC-specific knockout of FFAR4 aggravated renal function and pathological damage, whereas FFAR4 activation by TUG-891 alleviated the severity of disease in cisplatin-induced AKI mice. Notably, FFAR4, as a key determinant, was firstly explored to regulate cellular senescence both in injured kidneys of AKI mice and TECs, which was indicated by senescence-associated β-galactosidase (SA-β-gal) activity, marker protein p53, p21, Lamin B1, phospho-histone H2A.X, phospho-Rb expression, and secretory phenotype IL-6 level. Mechanistically, pharmacological activation and overexpression of FFAR4 reversed the decrease of aging-related SirT3 protein, where FFAR4 regulated SirT3 expression to exhibit anti-senescent effect via Gq subunit-mediated CaMKKβ/AMPK signaling in cisplatin-induced mice and TECs. These findings highlight the original role of tubular FFAR4 in cellular senescence via AMPK/SirT3 signaling and identify FFAR4 as a potential drug target against AKI.
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