CAV1 Exacerbates Renal Tubular Epithelial Cell Senescence by Suppressing CaMKK2/AMPK-Mediated Autophagy.

Liya Sun, Lujun Xu, Tongyue Duan, Yiyun Xi, Zebin Deng, Shilu Luo, Chongbin Liu, Chen Yang, Huafeng Liu, Lin Sun

Department of Nephrology, Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.Department of Nephrology, Key Laboratory of Kidney Disease and Blood Purification, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China. · pubmed

Paper

Abstract

Renal proximal tubular epithelial cell (PTEC) senescence and defective autophagy contribute to kidney aging, but the mechanisms remain unclear. Caveolin-1 (CAV1), a crucial component of cell membrane caveolae, regulates autophagy and is associated with cellular senescence. However, its specific role in kidney aging is poorly understood. In this study, we generated Cav1 gene knockout mice and induced kidney aging using D-galactose (D-gal). The results showed that CAV1 expression increased in the renal cortex of the aging mice, which was accompanied by exacerbated renal interstitial fibrosis, elevated levels of senescence-associated proteins γH2AX and p16

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Research summary

CAV1 exacerbates renal tubular epithelial cell senescence by suppressing CaMKK2/AMPK-mediated autophagy. This study addresses the mechanisms of cellular senescence and autophagy in kidney aging, which are critical factors in the broader context of aging and age-related diseases.

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