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血管内皮细胞分泌的外泌体通过促进软骨细胞凋亡促进骨关节炎发病机制。

Vascular endothelial cell-secreted exosomes facilitate osteoarthritis pathogenesis by promoting chondrocyte apoptosis.

机构信息

Department of Clinic of Spine Center, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200082, China.

出版信息

Aging (Albany NY). 2021 Feb 1;13(3):4647-4662. doi: 10.18632/aging.202506.

DOI:10.18632/aging.202506
PMID:33526719
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7906201/
Abstract

Exosomes are major mediators of cell-to-cell communication, and are involved in many physiological and pathological processes. Recently, the roles of exosomes in osteoarthritis (OA) and their therapeutic potential have received increasing attention. Exosomes derived from vascular endothelial cells have been confirmed to participate in the occurrence and development of numerous diseases; however, their effects in OA have not been reported. Here, we demonstrated the roles of exosomes secreted by vascular endothelial cells in the development of OA. Through and experiments, we demonstrated that exosomes derived from vascular endothelial cells decreased the ability of chondrocytes to resist oxidative stress by inhibiting autophagy and p21 expression, thereby increasing the cellular ROS content and inducing apoptosis. These findings indicate that exosomes derived from vascular endothelial cells promote the progression of OA, thus, providing new ideas for the diagnosis and treatment of OA.

摘要

外泌体是细胞间通讯的主要介质,参与许多生理和病理过程。最近,外泌体在骨关节炎(OA)中的作用及其治疗潜力受到了越来越多的关注。已经证实,来源于血管内皮细胞的外泌体参与了许多疾病的发生和发展;然而,它们在 OA 中的作用尚未报道。在这里,我们证明了血管内皮细胞分泌的外泌体在 OA 发展中的作用。通过 和 实验,我们证明了来源于血管内皮细胞的外泌体通过抑制自噬和 p21 表达降低了软骨细胞抵抗氧化应激的能力,从而增加了细胞内 ROS 含量并诱导了细胞凋亡。这些发现表明,血管内皮细胞来源的外泌体促进了 OA 的进展,为 OA 的诊断和治疗提供了新的思路。

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