title: Lack of oxygen in articular cartilage: consequences for chondrocyte biology.
abstract: Controlling the chondrocytes phenotype remains a major issue for cartilage repair strategies. These cells are crucial for the biomechanical properties and cartilage integrity because they are responsible of the secretion of a specific matrix. But chondrocyte dedifferentiation is frequently observed in cartilage pathology as well as in tissue culture, making their study more difficult. Given that normal articular cartilage is hypoxic, chondrocytes have a specific and adapted response to low oxygen environment. While huge progress has been performed on deciphering intracellular hypoxia signalling the last few years, nothing was known about the particular case of the chondrocyte biology in response to hypoxia. Recent findings in this growing field showed crucial influence of the hypoxia signalling on chondrocytes physiology and raised new potential targets to repair cartilage and maintain tissue integrity. This review will thus focus on describing hypoxia-mediated chondrocyte function in the native articular cartilage.
authors.affiliation: The Kennedy Institute of Rheumatology, Faculty of Medicine, Imperial College London, 65 Aspenlea Road, London W6 8LH, UK. j.lafont@imperial.ac.uk
authors.forename: Jérôme E
authors.initials: JE
authors.lastname: Lafont
mesh_terms: D002358:Cartilage, Articular / Q000737:chemistry / Q000378:metabolism*; D002454:Cell Differentiation; D015687:Cell Hypoxia; D019902:Chondrocytes / Q000166:cytology* / Q000378:metabolism; D049308:Dioxygenases / Q000378:metabolism; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism
chemical_list: C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D049308:Dioxygenases; D010100:Oxygen
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