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. 2022 Jul 14;9(8):1224–1240. doi: 10.1002/acn3.51624

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© 2022 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Schematic diagram of enhanced RCAN1.4 by HIF1α in astrocytes under OGD conditions. RCAN1.4 inhibits postischemic inflammation in astrocytes via inhibition of the NF‐κB signaling pathway. Activation of OGD results in upregulation of HIF1α in the nucleus, and HIF1α interacts with the specific HRE in the RCAN1.4 promoter, initiating its transcription. By inhibiting the phosphorylation and degradation of IκBα protein, RCAN1.4 suppresses NF‐κB/p65 nuclear translocation, subsequently alleviating postischemic inflammation in astrocytes. OGD, oxygen–glucose deprivation; RCAN1.4, the isoform 4 of regulator of calcineurin 1.