Research progression in the pathogenesis of osteoarthritis.
10.12200/j.issn.1003-0034.2021.10.018
- Author:
Jin-Shuo TANG
1
;
Zhong-Sheng ZHOU
1
;
Jian-Lin XIAO
1
;
Zhong-Li GAO
1
;
Jian-Lin ZUO
1
Author Information
1. Department of Orthopaedics and Joint, China-Japan Union Hospital of Jilin University, Changchun 130031, Jilin, China.
- Publication Type:Journal Article
- Keywords:
Osteoarthritis;
Pathogenesis;
Review literature
- MeSH:
Cartilage;
Cartilage, Articular;
Chondrocytes;
Humans;
Interleukin-1beta;
Osteoarthritis/genetics*;
Signal Transduction;
Tumor Necrosis Factor-alpha
- From:
China Journal of Orthopaedics and Traumatology
2021;34(10):985-990
- CountryChina
- Language:Chinese
-
Abstract:
Osteoarthritis(OA) is one of the most common joint diseases. As Chinese society enters the age of aging, the incidence of OA has been soar year by year, and research on its pathogenesis has been continuously valued by researchers. Studies have found that inflammatory cytokines, mainly interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), were responsible for the construction of OA inflammatory networks. It was also found that the overexpression of proteases, mainly matrix metalloproteinases(MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), was the direct cause of OA cartilage deficiency. What's more, signaling pathways such as stromal cell derived factor-1 (SDF-1) and Wnt, chondrocytic senescence and the senescence-associated secretory phenotype (SASP), chondrocyte apoptosis and autophagy, and estrogen all play significant roles in OA pathogenesis. This paper extensively reviews the research literature relevant to the pathogenesis of OA in recent years, and systematically expounds the pathogenesis of OA from two aspects:molecular level and cell level. At the end of the paper, we discussed and predicted some potential directions in the future clinical diagnosis and treatment of OA.
