Noncanonical function of Pannexin1 promotes cellular senescence and renal fibrosis post-acute kidney injury.

Liuwei Huang, Yanting Shen, Xiaoling Pan, Jiaqi Li, Caizhen Li, Lixin Ruan, Sitan He, Lanlan Huang, Kangyi Liu, Xin Zhao, Jian Geng, Jie Guo, Fan Fan Hou, Jun Wang

Division of Nephrology, National Key Laboratory for Prevention and Treatment of Multi-organ Injury, Nanfang Hospital, Southern Medical University, Guangzhou, China. · pubmed

Paper

Abstract

Acute kidney injury (AKI) can lead to chronic kidney disease (CKD), a transition driven by cellular senescence, a state of irreversible cell-cycle arrest. However, the molecular mechanisms promoting this pathological process remain unclear. Here we show that the channel protein Pannexin1 (Panx1) promotes this detrimental senescence and subsequent kidney fibrosis. We found that Panx1 functions in a noncanonical role as a calcium (Ca

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Research summary

Pannexin1 promotes cellular senescence and renal fibrosis following acute kidney injury. The study addresses the mechanisms of cellular senescence, which is a key process in aging and age-related diseases, particularly in the context of kidney health.

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