The Pro-Inflammatory Cytokine IL6 Suppresses Mitochondrial Function Via the Gp130-Jak1/stat1/3-hif1α/errα Axis.

Jianing Xu,Matthew Wakai, Kun Xiong, Yanfeng Yang, Adithya Prabakaran, Sophia Wu, Diana Ahrens, Maria Del Pilar Molina-Portela,Min Ni,Yu Bai,Tea Shavlakadze,David J Glass

Cell Reports（2025）SCI 4区

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Abstract

Chronic inflammation and a decline in mitochondrial function are hallmarks of aging. Here, we show that the two mechanisms may be linked. We found that interleukin-6 (IL6) suppresses mitochondrial function in settings where PGC1 (both PGC1α and PGC1β) expression is low. This suppression is mediated by the JAK1/STAT1/3 axis, which activates HIF1α through non-canonical mechanisms involving upregulation of HIF1A and ERRα transcription, and subsequent stabilization of the HIF1A protein by ERRα. HIF1α, in turn, inhibits ERRα, which is a master regulator of mitochondrial biogenesis, thus contributing to the inhibition of mitochondrial function. When expressed at higher levels, PGC1 rescues ERRα to boost baseline mitochondrial respiration, including under IL6-treated conditions. Our study suggests that inhibition of the IL6 signaling axis could be a potential treatment for those inflammatory settings where mitochondrial function is compromised.

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