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p38MAPK Signaling Pathway in Osteoarthritis Pathological and Therapeutic Aspects

期刊

JOURNAL OF INFLAMMATION RESEARCH
卷 15, 期 -, 页码 723-734

出版社

DOVE MEDICAL PRESS LTD
DOI: 10.2147/JIR.S348491

关键词

osteoarthritis; p38MAPK signaling pathway; aging; inflammation

资金

  1. National Natural Science Foundation of China [81902303]
  2. Natural Science Foundation of Hunan Province [2020JJ8043]
  3. Guangdong Basic and Applied Basic Research Foundation [2020A151501048]
  4. Key project of Hunan Provincial Health Commission [20201902]
  5. Project of Hunan Provincial Health Commission [c2019133]
  6. Shenzhen Science and Technology Project [JCYJ20190806164216661, RCBS20200714114856299]
  7. Science and Technology Project of Changsha City [kq2004165]
  8. Hunan Provincial Clinical Medical Technology Innovation Guiding Project [2020SK53307]
  9. Clinical Research Project of Shenzhen Second People's Hospital [20203357028]

向作者/读者索取更多资源

Osteoarthritis (OA) is an aging-related joint disease. The p38MAPK signaling pathway plays an important role in the pathogenesis and progression of OA, and its inhibition shows potential therapeutic effects.
Osteoarthritis (OA) is an aging-related joint disease, pathologically featured with degenerated articular cartilage and deformation of subchondral bone. OA has become the fourth major cause of disability in the world, imposing a huge economic burden. At present, the pathogenesis and pathophysiology of OA are still unclear. Complex regulating networks containing different biochemical signaling pathways are involved in OA pathogenesis and progression. The p38MAPK signaling pathway is a member of the MAPK signaling pathway family, which participates in the induction of cellular senescence, the differentiation of chondrocytes, the synthesis of matrix metalloproteinase (MMPs) and the production of pro-inflammatory factors. In recent years, studies on the regulating role of p38MAPK signaling pathway and the application of its inhibitors have attracted growing attention, with an increasing number of in vivo and in vitro studies. One interesting finding is that the inhibition of p38MAPK could suppress chondrocyte inflammation and ameliorate OA, indicating its therapeutic role in OA treatment. Based on this, we reviewed the mechanisms of p38MAPK signaling pathway in the pathogenesis of OA, hoping to provide new ideas for future research and OA treatment.

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