ArticleThe Journal of clinical investigation2019
Calcium channel Orai1 promotes lymphocyte IL-17 expression and progressive kidney injury.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 57 citations in OpenAlex.
- T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- CRAC channels as targets for immunotherapy.Current opinion in immunology · 2026Review
- STIM/Orai-Mediated Store-Operated CaCells · 2026Review
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Tetramethylpyrazine alleviates acute kidney injury by activating the Wnt/β-catenin pathway independent of DKK1.Experimental and therapeutic medicine · 2025Article
- Navigating the Complex Pathogenesis of Acute Kidney Injury: Exploring Macrophage Dynamics, Mitochondrial Dysfunction, and Ferroptosis Pathways.Advances in kidney disease and health · 2025Review
- Splenectomy modulates intrarenal B cell differentiation and impairs repair of post-ischemic kidney.Frontiers in immunology · 2025Article
- Lymphocytes and innate immune cells in acute kidney injury and repair.Nature reviews. Nephrology · 2024Review
- Exploring diagnostic biomarkers of type 2 cardio-renal syndrome based on secreted proteins and bioinformatics analysis.Scientific reports · 2024Article
- Double-negative T cells have a reparative role after experimental severe ischemic acute kidney injury.American journal of physiology. Renal physiology · 2024Article
- Subcutaneous injection of adipose stromal cell-secretome improves renal function and reduces inflammation in established acute kidney injury.Stem cell research & therapy · 2024Article
- Impaired hemodynamic renal reserve response following recovery from established acute kidney injury and improvement by hydrodynamic isotonic fluid delivery.American journal of physiology. Renal physiology · 2024Article
- Targeting inerleukin-6 for renoprotection.Frontiers in immunology · 2024Review
- Novel insights into STIM1's role in store-operated calcium entry and its implications for T-cell mediated inflammation in trigeminal neuralgia.Frontiers in molecular neuroscience · 2024Article
- Pathway from Acute Kidney Injury to Chronic Kidney Disease: Molecules Involved in Renal Fibrosis.International journal of molecular sciences · 2023Review
- IL-17C neutralization protects the kidney against acute injury and chronic injury.EBioMedicine · 2023Article
- Article
- T CellAntioxidants & redox signaling · 2023Article
- Enhanced Orai1-mediated store-operated CaThe Journal of biological chemistry · 2022Article
- Role of T cells in ischemic acute kidney injury and repair.The Korean journal of internal medicine · 2022Review
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
We hypothesized that the store-operated calcium entry (SOCE) channel, Orai1, participates in the activation of Th17 cells and influences renal injury. In rats, following renal ischemia/reperfusion (I/R), there was a rapid and sustained influx of Orai1+ CD4 T cells and IL-17 expression was restricted to Orai1+ cells. When kidney CD4+ cells of post-acute kidney injury (post-AKI) rats were stimulated with angiotensin II and elevated Na+ (10-7 M/170 mM) in vitro, there was an enhanced response in intracellular Ca2+ and IL-17 expression, which was blocked by SOCE inhibitors 2APB, YM58483/BTP2, or AnCoA4. In vivo, YM58483/BTP2 (1 mg/kg) attenuated IL-17+ cell activation, inflammation, and severity of AKI following either I/R or intramuscular glycerol injection. Rats treated with high-salt diet (5-9 weeks after I/R) manifested progressive disease indicated by enhanced inflammation, fibrosis, and impaired renal function. These responses were significantly attenuated by YM58483/BTP2. In peripheral blood of critically ill patients, Orai1+ cells were significantly elevated by approximately 10-fold and Th17 cells were elevated by approximately 4-fold in AKI versus non-AKI patients. Further, in vitro stimulation of CD4+ cells from AKI patients increased IL-17, which was blocked by SOCE inhibitors. These data suggest that Orai1 SOCE is a potential therapeutic target in AKI and CKD progression.
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