Longevity & AgingKidney Channel Protein Drives Aging and Fibrosis After Acute Kidney Injury
Researchers at Southern Medical University discovered that Pannexin1 (Panx1), a channel protein found in kidney tubule cells, plays an unexpected role inside the endoplasmic reticulum (ER) — leaking calcium onto mitochondria, causing overload, dysfunction, and pro-senescence signals. Using mouse models of acute kidney injury (AKI) and human kidney tissue, they showed that elevated Panx1 drives tubular cell senescence and subsequent kidney fibrosis, the hallmarks of the AKI-to-chronic kidney disease (CKD) transition. Deleting the Panx1 gene in mice significantly reduced both senescence and fibrosis. These findings position ER-resident Panx1 as a novel and potentially druggable driver of kidney disease progression.
