ArticleThe Journal of clinical investigation2019
Orai1: CRACing the Th17 response in AKI.
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. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Exploring diagnostic biomarkers of type 2 cardio-renal syndrome based on secreted proteins and bioinformatics analysis.Scientific reports · 2024Article
- Clinical and pathological significance of Orai1 channel expression in human diabetic nephropathy.Kidney research and clinical practice · 2024Article
- The effect ofTranslational andrology and urology · 2024Article
- Article
- IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells.Cellular and molecular life sciences : CMLS · 2023Article
- The role of ion channels in T cell function and disease.Frontiers in immunology · 2023Review
- Stratifin promotes renal dysfunction in ischemic and nephrotoxic AKI mouse models via enhancing RIPK3-mediated necroptosis.Acta pharmacologica Sinica · 2022Article
- Calcium Signaling in T Cells and Chronic Inflammatory Disorders of the Oral Cavity.Journal of dental research · 2021Review
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1 author at 1 institution in 1 country.
Funding
Abstract
A strong Th17 inflammatory response aggravates ischemia reperfusion-induced (IR-induced) acute kidney injury (AKI), tissue fibrosis, and AKI-to-chronic kidney disease (CKD) progression. However, the underlying mechanisms of sustained Th17 activation following AKI and during AKI-to-CKD progression are unclear. In this issue of the JCI, Mehrotra et al. present compelling evidence that the store-operated calcium (Ca2+) channel Orai1 sustains Th17-driven inflammatory response after AKI and drives the AKI-to-CKD transition. Orai1 blockade significantly protected renal function from IR, attenuated high-salt-induced AKI-to-CKD progression in rats, and decreased Th17 response in rat and human T cells. Therapeutic targeting of Orai1 can potentially reduce AKI, AKI-to-CKD progression, and other Th17-driven diseases.
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Registered trials
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 OpenQuestion graph.