Molecular mechanisms and potential applications of chondroitin sulphate in managing post-traumatic osteoarthritis.
Iryna GolovachDmytro RekalovOleh Ye AkimovHeorhii KostenkoViktoriia KostenkoArtur MishchenkoNatalia SolovyovaVitalii KostenkoPublished in: Reumatologia (2023)
Post-traumatic osteoarthritis (PTOA), a disorder of the synovium, subchondral bone, and cartilage that affects the entire joint, constitutes approximately 12% of all cases of symptomatic osteoarthritis. This review summarizes the pathogenetic mechanisms that underlie the positive influence of chondroitin sulphates (CSs) on PTOA as means of preventive and therapeutic treatment. Mechanisms of PTOA development involve chondrocytes undergoing various forms of cell death (apoptosis, pyroptosis, necroptosis, ferroptosis and/or necrosis). Chondroitin sulphates are a class of glycosaminoglycans that improve the structure and function of cartilage and subchondral bone, which is associated with their ability to decrease the activation of NF-κB and p38 MAPK, and up-regulate Nrf2. Standardized small fish extract (SSFE) is an example of the drugs that can attenuate NF-κB-mediated systemic inflammation, potentially helping to reduce joint inflammation and cartilage degradation, improve joint function, and alleviate pain and disability in patients with these conditions.
Keyphrases
- oxidative stress
- cell death
- extracellular matrix
- cell cycle arrest
- rheumatoid arthritis
- hyaluronic acid
- knee osteoarthritis
- signaling pathway
- bone mineral density
- pi k akt
- lps induced
- multiple sclerosis
- chronic pain
- soft tissue
- bone loss
- nuclear factor
- neuropathic pain
- endoplasmic reticulum stress
- bone regeneration
- cell proliferation
- spinal cord