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Osteoarthritis: Role of Peroxisome Proliferator-Activated Receptors

Overview
Journal Int J Mol Sci
Publisher MDPI
Date 2023 Sep 9
PMID 37685944
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Abstract

Osteoarthritis (OA) represents the foremost degenerative joint disease observed in a clinical context. The escalating issue of population aging significantly exacerbates the prevalence of OA, thereby imposing an immense annual economic burden on societies worldwide. The current therapeutic landscape falls short in offering reliable pharmaceutical interventions and efficient treatment methodologies to tackle this growing problem. However, the scientific community continues to dedicate significant efforts towards advancing OA treatment research. Contemporary studies have discovered that the progression of OA may be slowed through the strategic influence on peroxisome proliferator-activated receptors (PPARs). PPARs are ligand-activated receptors within the nuclear hormone receptor family. The three distinctive subtypes-PPARα, PPARβ/δ, and PPARγ-find expression across a broad range of cellular terminals, thus managing a multitude of intracellular metabolic operations. The activation of PPARγ and PPARα has been shown to efficaciously modulate the NF-κB signaling pathway, AP-1, and other oxidative stress-responsive signaling conduits, leading to the inhibition of inflammatory responses. Furthermore, the activation of PPARγ and PPARα may confer protection to chondrocytes by exerting control over its autophagic behavior. In summation, both PPARγ and PPARα have emerged as promising potential targets for the development of effective OA treatments.

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References
1.
Konttinen Y, Ainola M, Valleala H, Ma J, Ida H, Mandelin J . Analysis of 16 different matrix metalloproteinases (MMP-1 to MMP-20) in the synovial membrane: different profiles in trauma and rheumatoid arthritis. Ann Rheum Dis. 1999; 58(11):691-7. PMC: 1752794. DOI: 10.1136/ard.58.11.691. View

2.
Kang X, Yang Z, Sheng J, Liu J, Xie Q, Zheng W . Oleanolic acid prevents cartilage degeneration in diabetic mice via PPARγ associated mitochondrial stabilization. Biochem Biophys Res Commun. 2017; 490(3):834-840. DOI: 10.1016/j.bbrc.2017.06.127. View

3.
Nogueira-Recalde U, Lorenzo-Gomez I, Blanco F, Loza M, Grassi D, Shirinsky V . Fibrates as drugs with senolytic and autophagic activity for osteoarthritis therapy. EBioMedicine. 2019; 45:588-605. PMC: 6642320. DOI: 10.1016/j.ebiom.2019.06.049. View

4.
Moreno M, Lombardi A, Silvestri E, Senese R, Cioffi F, Goglia F . PPARs: Nuclear Receptors Controlled by, and Controlling, Nutrient Handling through Nuclear and Cytosolic Signaling. PPAR Res. 2010; 2010. PMC: 2929508. DOI: 10.1155/2010/435689. View

5.
Kersten S, Desvergne B, Wahli W . Roles of PPARs in health and disease. Nature. 2000; 405(6785):421-4. DOI: 10.1038/35013000. View