ArticleRedox biology2024
FAM3A plays a key role in protecting against tubular cell pyroptosis and acute kidney injury.
Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Berberrubine alleviates PCS-induced tubular injury via HNRNPF/NR4A1/ER stress axis.Acta pharmacologica Sinica · 2026Article
- Delaying Stress Granule Disassembly by PARG Inhibition Attenuates Renal Tubular Cell Pyroptosis in Acute Kidney Injury.International journal of molecular sciences · 2026Article
- Review
- 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
- Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Andrographolide Suppresses Influenza A Virus-Induced Pyroptosis via PI3K/AKT-Mediated Caspase-3/GSDME Inactivation.Biomedicines · 2026Article
- Immune molecular mechanisms of PANoptosis in sepsis-induced acute kidney injury.Inflammation and regeneration · 2026Review
- Acute kidney injury over the past decade: from definition evolution to pathogenesis insights and innovative therapeutic strategies.Cellular and molecular life sciences : CMLS · 2026Review
- Animal models of critical illness in the Asia-Pacific region: current practices, shared challenges, and future directions.Intensive care medicine experimental · 2026Review
- Organelle stress in NLRP3 inflammasome: a central mediator of neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- Integrative omics and experimental validation reveal METTL17 and SLC27A1 as biomarkers and potential therapeutic targets in chronic kidney disease.Frontiers in immunology · 2026Article
- Cell-state- and compartment-dependent PI3K/Akt redox signaling in chronic kidney disease: mechanisms and translational implications.Frontiers in pharmacology · 2026Review
- Navigating renal safety in the biologic treatment of psoriasis: from immunologic mechanisms to clinical practice.Frontiers in immunology · 2026Review
- Panax Notoginseng Saponins Inhibit Apoptosis and Alleviate Renal Ischemia-Reperfusion Injury Through the ROCK2/NF-κB Pathway.Molecular biotechnology · 2026Article
- Targeting cGAS-STING-macrophage axis: a novel therapeutic horizon for renal fibrosis.Frontiers in immunology · 2026Review
- A pH-Responsive Biomimetic Antioxidant Nanoplatform with Dual Renal Targeting for Synergistic Therapy of Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- FAM3A drives uncoupling of muscle lipid accumulation and insulin resistance depending on insulin receptor.Cell death & disease · 2025Article
- Dapagliflozin ameliorates kidney injury following limb ischemia-reperfusion via the AMPK/SIRT1/NLRP3 pathway.Renal failure · 2025Article
- Salidroside Alleviates Renal Ischemia-reperfusion Injury by Inhibiting Macrophage Pyroptosis Through HIF Signaling.Inflammation · 2025Article
- Sodium aescinate protects renal ischemia-reperfusion and pyroptosis through AKT/NLRP3 signaling pathway.Renal failure · 2025Article
Corrections and comments
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Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is in high prevalence worldwide but with no therapeutic strategies. Programmed cell death in tubular epithelial cells has been reported to accelerate a variety of AKI, but the major pathways and underlying mechanisms are not defined. Herein, we identified that pyroptosis was responsible for AKI progression and related to ATP depletion in renal tubular cells. We found that FAM3A, a mitochondrial protein that assists ATP synthesis, was decreased and negatively correlated with tubular cell injury and pyroptosis in both mice and patients with AKI. Knockout of FAM3A worsened kidney function decline, increased macrophage and neutrophil cell infiltration, and facilitated tubular cell pyroptosis in ischemia/reperfusion injury model. Conversely, FAM3A overexpression alleviated tubular cell pyroptosis, and inhibited kidney injury in ischemic AKI. Mechanistically, FAM3A promoted PI3K/AKT/NRF2 signaling, thus blocking mitochondrial reactive oxygen species (mt-ROS) accumulation. NLRP3 inflammasome sensed the overload of mt-ROS and then activated Caspase-1, which cleaved GSDMD, pro-IL-1β, and pro-IL-18 into their mature forms to mediate pyroptosis. Of interest, NRF2 activator alleviated the pro-pyroptotic effects of FAM3A depletion, whereas the deletion of NRF2 blocked the anti-pyroptotic function of FAM3A. Thus, our study provides new mechanisms for AKI progression and demonstrates that FAM3A is a potential therapeutic target for treating AKI.
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