tailieunhanh - Báo cáo y học: "Cartilage homeostasis in health and rheumatic diseases"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Cartilage homeostasis in health and rheumatic diseases. | Available online http content 11 3 224 Review Cartilage homeostasis in health and rheumatic diseases Mary B Goldring1 and Kenneth B Mareu2 3 1 Research Division Hospital for Special Surgery affiliated with Weill College of Medicine of Cornell University Caspary Research Building 535 E. 70th Street New York NY 10021 USA 2Biochemistry and Cell Biology Department Stony Brook University Life Sciences Rm 330 Stony Brook NY 11794 USA 3Centro Ricerca Biomedica Applicata S. Orsola-Malpighi University Hospital University of Bologna Via Massarenti 9 40138 Bologna Italy Corresponding author Mary B Goldring goldringm@ Published 19 May 2009 This article is online at http content 11 3 224 2009 BioMed Central Ltd Arthritis Research Therapy 2009 11 224 doi ar2592 Abstract As the cellular component of articular cartilage chondrocytes are responsible for maintaining in a low-turnover state the unique composition and organization of the matrix that was determined during embryonic and postnatal development. In joint diseases cartilage homeostasis is disrupted by mechanisms that are driven by combinations of biological mediators that vary according to the disease process including contributions from other joint tissues. In osteoarthritis OA biomechanical stimuli predominate with upregulation of both catabolic and anabolic cytokines and recapitulation of developmental phenotypes whereas in rheumatoid arthritis RA inflammation and catabolism drive cartilage loss. In vitro studies in chondrocytes have elucidated signaling pathways and transcription factors that orchestrate specific functions that promote cartilage damage in both OA and RA. Thus understanding how the adult articular chondrocyte functions within its unique environment will aid in the development of rational strategies to protect cartilage from damage resulting from joint disease. This review will cover current knowledge about the specific cellular and biochemical

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