ZDHHC11-mediated palmitoylation alleviates chondrocyte senescence and serves as a therapeutic target for osteoarthritis.

Kefan Wang, Wei He, Zhe Gong, Jun Gao, Tianyou Gao, Nan Pan, Dongze Wu, Yijie Yang, Zhuang Li, Xing Zhao, Mingliang Ji, Shuying Shen

Department of Orthopedic Surgery, Sir Run Run Shaw Hospital, Medical College of Zhejiang University, Hangzhou, China. · pubmed

Paper

Abstract

Osteoarthritis (OA) is a whole-joint disorder that interferes with the quality of life in older individuals. Here we report that ZDHHC11 is highly expressed in articular chondrocytes but is downregulated in the degenerated cartilage of aged mice and patients with OA. ZDHHC11 prevents chondrocyte senescence and promotes cartilage anabolism, culminating in an improved OA phenotype. The deletion of Zdhhc11 in mice (Zdhhc11

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

ZDHHC11 prevents chondrocyte senescence and promotes cartilage anabolism, which may improve osteoarthritis outcomes. The study addresses a mechanism related to cellular aging in chondrocytes, linking it to a common age-related disease, thus contributing to the understanding of aging processes.

Author of this paper? Send a correction.