Open AccessCCAL1 enhances osteoarthritis through the NF‐κB/AMPK signaling pathway
Author(s) -
Zhu Hanzhong,
Yan Hongyu,
Ma Junan,
Zhang Hua,
Zhang Jidong,
Hu Zhiheng,
Guo Yunliang
Publication year - 2020
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12989
Subject(s) - ampk , signal transduction , nf κb , cancer research , osteoarthritis , caffeic acid phenethyl ester , chemistry , microbiology and biotechnology , activator (genetics) , viability assay , receptor , apoptosis , protein kinase a , phosphorylation , medicine , biology , biochemistry , pathology , alternative medicine , caffeic acid , antioxidant
CCAL1, a member of the tumor necrosis factor receptor superfamily 11B, encodes osteoprotegerin. We report that CCAL1 is highly expressed in osteoarthritis (OA) tissues and Human Chondrocyte‐Osteoarthritis (HC‐OA) cells and its expression level is positively correlated with the severity of OA. CCAL1 could activate NF‐κB and inhibit AMPK pathways to promote HC‐OA cell fibrosis, viability and proliferation.