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Crosstalk between programmed cell death in chondrocytes-a molecular mechanism of osteoarthritis
Kun Zhang1, Lianlin Zeng1, Huiqin Min2
1Department of Rehabilitation Medicine, Suining Central Hospital, Suining, Sichuan Province, China.
Abstract:
The pathogenesis of osteoarthritis (OA), particularly knee osteoarthritis, is unknown, which is a chronic inflammatory systemic disease. Pathologically, the disease is primarily defined by alterations including cartilage degeneration and joint space decrease, which can result in joint deformity and loss of function. While the drugs currently used to treat OA can be helpful, their adverse effects are so obvious that they need to be further modified. Therefore, a detailed analysis of the mechanisms underlying the initiation and progression of OA is necessary to identify novel treatment targets. Much emphasis has been paid to the significant role that programmed cell death (PCD) plays in OA, particularly in chondrocytes and synoviocytes, where PCD is particularly dysregulated. This paper summarizes the regulatory roles of several types of PCD in OA, including the apoptosis, necroptosis, and autophagy as well as the more recently identified NETosis, pyroptosis, ferroptosis, and cuproptosis. We also discuss the regulatory roles of these processes in chondrocytes, synoviocytes, and other cells. These findings not only provide a vital theoretical basis for enhancing clinical OA treatment practices, but they also point the way toward the development of new target drugs.
Insights
Programmed cell death (PCD) pathways are dysregulated in osteoarthritis (OA), impacting cartilage and joint health. Understanding these mechanisms, including apoptosis, necroptosis, and ferroptosis, is crucial for developing new OA treatments.
Area of Science:
- Biomedical Science
- Rheumatology
- Cell Biology
Background:
- Osteoarthritis (OA) is a chronic inflammatory disease characterized by cartilage degeneration and joint dysfunction.
- Current OA treatments have limitations and significant adverse effects, necessitating novel therapeutic targets.
- Programmed cell death (PCD) is increasingly recognized as a key factor in OA pathogenesis, particularly in chondrocytes and synoviocytes.
Purpose of the Study:
- To analyze the mechanisms underlying osteoarthritis initiation and progression.
- To summarize the regulatory roles of various programmed cell death (PCD) types in OA.
- To identify novel therapeutic targets for OA treatment.
Main Methods:
- Literature review and synthesis of existing research on PCD in OA.
- Analysis of the roles of apoptosis, necroptosis, autophagy, NETosis, pyroptosis, ferroptosis, and cuproptosis in OA.
- Discussion of PCD mechanisms in chondrocytes, synoviocytes, and other relevant cells.
Main Results:
- Programmed cell death (PCD) pathways are significantly dysregulated in osteoarthritis (OA).
- Specific PCD types, including apoptosis, necroptosis, autophagy, NETosis, pyroptosis, ferroptosis, and cuproptosis, play distinct regulatory roles in OA.
- These PCD processes are implicated in the pathology of chondrocytes, synoviocytes, and other joint-resident cells.
Conclusions:
- Dysregulated programmed cell death (PCD) is a critical component of osteoarthritis (OA) pathogenesis.
- Understanding the multifaceted roles of different PCD pathways offers a vital theoretical basis for improving OA treatment.
- Targeting specific PCD mechanisms presents a promising avenue for the development of novel OA therapeutics.
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