Orai1: CRACing the Th17 response in AKI

Research output: Contribution to journalReview articlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)4583-4586
Number of pages4
JournalJournal of Clinical Investigation
Issue number11
StatePublished - Nov 1 2019

ASJC Scopus subject areas

  • Medicine(all)


Dive into the research topics of 'Orai1: CRACing the Th17 response in AKI'. Together they form a unique fingerprint.

Cite this