TASK-2/14-3-3ε pathway promotes renal fibrosis by driving mitochondrial peripheral fission

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TASK-2/14-3-3ε pathway promotes renal fibrosis by driving mitochondrial peripheral fission

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Co-author 1

Nana Song nanasong1129@163.com Zhongshan Hospital, Fudan University Department of Nephrology Shanghai China -

Co-author 2

Xiaoqiang Ding ding.xiaoqiang@zs-hospital.sh.cn Zhongshan Hospital, Fudan University Department of Nephrology Shanghai China -

Co-author 3

Shengzhuo You youshengzhuo2001@163.com Zhongshan Hospital, Fudan University Department of Nephrology Shanghai China *

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Introduction

Intracellular potassium imbalance plays a critical yet underappreciated role in the progression of renal fibrosis. Our previous studies identified that excessive activation of the potassium channel TASK-2 induces intracellular hypokalemia and G2/M cell cycle arrest in renal tubular epithelial cells, thereby aggravating renal fibrosis. However, the underlying mechanisms remain unclear.

Methods

Wild-type C57 mice, TASK-2 cKO mice were used for in vivo studies.Unilateral Ishcehmia-Reperfusion (UIR) and Unilateral Ureteral Obstruction (UUO) mododel was applied to induce renal fibrosis.

Results

In the present study, transcriptomic analysis revealed that TASK-2 activation is associated with mitochondrial fission. Functional experiments demonstrated that inhibition of TASK-2 decreased Fis1 expression and reduced mitochondrial peripheral fission. Mechanistically, TASK-2–mediated intracellular potassium loss activated 14-3-3ε, which directly interacted with Fis1 and facilitated its mitochondrial localization. Knockdown or pharmacological inhibition of 14-3-3ε markedly attenuated TASK-2–induced mitochondrial peripheral fission, G2/M cell cycle arrest, and renal fibrosis. Conversely, inhibition of mitochondrial fission alleviated 14-3-3ε–induced G2/M arrest and fibrosis.

Conclusion

Collectively, these findings identify a novel TASK-2–14-3-3ε–Fis1 axis that links potassium imbalance to mitochondrial dynamics and fibrotic progression. TASK-2–mediated intracellular hypokalemia activates 14-3-3ε, which recruits Fis1 to mitochondria, driving peripheral fission and subsequent G2/M cell cycle arrest in renal tubular epithelial cells. This study provides new mechanistic insight into the role of potassium signaling in renal fibrosis and suggests potential therapeutic targets for CKD intervention.

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