Enolase 2-mediated lactylation-dependent disruption of the GNL3-MDM2-p53 axis in age-related osteoarthritis.

Feng Hua, Jiangyu Nan, Rong Wu, Bin Zhang, Qimeng Liu, Tianliang Ma, Zheyu Zhang, Yihe Hu, Jie Xie, Yute Yang

Department of Orthopedics, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China. · pubmed

Paper

Abstract

Age-related osteoarthritis (OA) involves metabolic dysregulation and chondrocyte senescence. This study examined the nonmetabolic role of enolase 2 (ENO2) in OA pathogenesis and its therapeutic potential.

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

The paper claims that enolase 2 mediates lactylation-dependent disruption of the GNL3-MDM2-p53 axis, contributing to the pathogenesis of age-related osteoarthritis. This research addresses a potential mechanism underlying age-related disease, focusing on metabolic dysregulation and cellular senescence, which are relevant to the aging process.

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