PINK1 overexpression suppresses p38 MAPK/NF‑κB signaling to attenuate chondrocyte senescence in osteoarthritis.

Lishi Jie, Yuanhui Zhang, Jiangyu Liu, Houyu Fu, Zaishi Zhu, Zeling Huang, Xiaoqing Shi, Peimin Wang, Songjiang Yin

Department of Orthopedics, The Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210029, P.R. China.Department of Orthopedics, The Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210029, P.R. China. · pubmed

Paper

Abstract

PTEN‑induced putative kinase 1 (PINK1), a master regulator of mitophagy, is implicated in mitochondrial homeostasis, yet its role in knee osteoarthritis (OA) pathogenesis remains unclear. The present study investigated the mechanisms by which PINK1 modulates chondrocyte senescence during OA progression. Utilizing a destabilization of the medial meniscus‑induced OA murine model, decreased PINK1 expression, impaired mitochondrial function and suppressed mitophagy were observed in OA cartilage.

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Research summary

PINK1 overexpression suppresses p38 MAPK/NF‑κB signaling to attenuate chondrocyte senescence in osteoarthritis. The study addresses the role of PINK1 in chondrocyte senescence, which is a key aspect of aging and age-related diseases, particularly in the context of osteoarthritis.

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