Interleukin-1β downregulates K + currents through K v 1.6 channels and promotes apoptosis by enhancing Ca 2+ influx in chondrocytes

American Journal of Physiology-Cell Physiology 2026

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Authors: Tomo Kurata, Yoshiaki Suzuki, Shinya Tateno, Shigeru Miyaki, Rubii Kondo, Eiva Bernotienė, Ali Mobasheri, Wayne R. Giles, Yuji Imaizumi, Hisao Yamamura
DOI: 10.1152/ajpcell.00381.2025
Cited by: 1
References: 63

Abstract

Our results reveal that K v 1.6 channels in mouse chondrocytes contribute to cell survival by regulating the resting membrane potential (RMP) and thus modulating intracellular Ca 2+ concentration ([Ca 2+ ] i ). Specifically, IL-1β can downregulate K v 1.6 channels and result in RMP depolarization, which increases Ca 2+ influx through Ca v 1.2 channels and promotes mitochondrial dysfunction and apoptosis. Downregulation of K v 1.6 channels was detected in chondrocytes of osteoarthritis (OA) model mice and OA patients. These findings suggest that K v 1.6 and/or Ca v 1.2 channels may be potential therapeutic targets for OA.

Fields of Study & Subjects

Osteoarthritis Treatment and Mechanisms Ion channel regulation and function Ion Channels and Receptors

Publication details

Journal / source
American Journal of Physiology-Cell Physiology
Publisher
American Physiological Society
Volume
330
Issue
4
Pages
C909–C925
Publication date
2 March 2026
Language
EN