Role of HIF-1? and HIF-2? in osteoarthritis - 13/05/15
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Abstract |
The hallmark of OA is cartilage destruction, several factors such as catabolic enzymes and chondrocyte death include apoptosis and/or autophagy are considered for the pathogenesis. Articular cartilage is maintained in a low oxygen environment throughout life. Chondrocytes are therefore adapted to these hypoxic conditions. The increased HIF-1α and HIF-2α mediate the response of chondrocytes to hypoxia. HIF-1α regulates chondrogenesis by regulating SOX9 expression in the genetic level, HIF-1 also serves to regulate both autophagy and apoptosis. Therefore, HIF-1α may protect articular cartilage by promoting the chondrocyte phenotype, maintaining chondrocyte viability, and supporting metabolic adaptation to a hypoxic environment. In contrast with HIF-1α, HIF-2α is a catabolic factor in the osteoarthritic process. Although HIF-2α is essential for hypoxic induction of the human articular chondrocyte phenotype, HIF-2α directly induces the expression of catabolic factors in chondrocytes, and HIF-2α enhances Fas expression to mediate chondrocyte apoptosis and regulates autophagy in maturing chondrocytes. Taken together, manipulation of HIF-1α and HIF-2α could represent a promising approach to the treatment of OA. Further study should elucidate the exact machnism of HIF-1α and HIF-2α in cartilage and determine which is predominant in osteoarthritic process.
Le texte complet de cet article est disponible en PDF.Keywords : HIF-1α, HIF-2α, Osteoarthritis, Apoptosis, Autophagy, Hypoxia
Plan
Vol 82 - N° 3
P. 144-147 - mai 2015 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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