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Accelerated aging in articular cartilage by ZMPSTE24 deficiency leads to osteoarthritis with impaired metabolic signaling and epigenetic regulation

Medicine and Health

Accelerated aging in articular cartilage by ZMPSTE24 deficiency leads to osteoarthritis with impaired metabolic signaling and epigenetic regulation

J. Suo, R. Shao, et al.

Discover how ZMPSTE24 deficiency is linked to osteoarthritis in an innovative study by Jinlong Suo and colleagues. This research unveils the intricate connection between aging, chondrocyte metabolism, and OA development, paving the way for potential new therapeutic strategies.

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Playback language: English
Abstract
Osteoarthritis (OA) is an age-related degenerative disease lacking disease-modifying therapies. This study investigates the role of ZMPSTE24 deficiency in OA development. Results show decreased *Zmpste24* expression in aging articular cartilage. *Zmpste24* knockout mice exhibited OA phenotypes, with transcriptome sequencing revealing that *Zmpste24* deletion or progerin accumulation affects chondrocyte metabolism, inhibits proliferation, and promotes senescence. The study elucidates the upregulation of H3K27me3 during chondrocyte senescence and the mechanism by which lamin A mutant stabilizes EZH2 expression. This aging-induced OA model provides a platform for discovering new OA therapeutics.
Publisher
Cell Death and Disease
Published On
May 22, 2023
Authors
Jinlong Suo, Rui Shao, Ruici Yang, Jinghui Wang, Zhong Zhang, Duo Wang, Ningning Niu, Xianyou Zheng, Weiguo Zou
Tags
Osteoarthritis
ZMPSTE24
Aging
Chondrocyte
Disease-modifying therapies
Senescence
Transcriptome sequencing

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