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作 者:Siming Dai Jiankun Fan Yue Zhang Zhenyong Hao Huiming Yu Zhiyi Zhang
机构地区:[1]Department of Rheumatology and Immunology,The First Affiliated Hospital of Harbin Medical University,Harbin,Heilongjiang 150001,China [2]The Laboratory of Medical Genetics,Harbin Medical University,Harbin,Heilongjiang 150001,China [3]Shenzhen Futian Hospital for Rheumatic Diseases,Shenzhen,Guangdong 518000,China [4]Department of Orthopedic Surgery of Harbin Fifth Hospital,Harbin,Heilongjiang 150001,China
出 处:《Chinese Medical Journal》2022年第1期92-94,共3页中华医学杂志(英文版)
基 金:This work was supported by grants from the National Natural Science Foundation of China(No.81771749 and No.81771748)。
摘 要:Osteoarthritis(OA)is a debilitating disease with limited treatment options.[1]Autophagy serves as an important protective mechanism against the deterioration of cartilage and is negatively regulated by the mammalian target of rapamycin(mTOR).[2]In previous studies,celastrol could promote autophagy in various cell types and had the promising therapeutic potential for OA.[3]However,the effect and underlying mechanisms of celastrol on autophagy in OA remain unclear.Our preliminary study using transcriptome sequencing and a network pharmacology analysis identified mTOR as a potential direct target of celastrol for protection against OA.[4]In this study,we aim to evaluate the effects of celastrol on mTOR activity in primary human osteoarthritic chondrocytes and to determine the mechanism by which it affects autophagy and endoplasmic reticulum(ER)stress.
关 键 词:protective MTOR OSTEOARTHRITIS
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