Response to Adiponectin associates with markers of cartilage degradation in osteoarthritis and induces production of proinflammatory and catabolic factors through mitogen-activated protein kinase pathways 英文参考文献.docVIP

Korkmaz Arthritis Research Therapy 2012, 14:402 /content/14/3/402 LETTER Response to ‘Adiponectin associates with markers of cartilage degradation in osteoarthritis and induces production of proin? ammatory and catabolic factors through mitogen-activated protein kinase pathways’ Cengiz Korkmaz* See related research by Koskinen et al., /content/13/6/R184 Di? erent mechanisms and mediators in di? erent stages of osteoarthritis (OA) may be involved in progression of the disease. Cross-sectional studies performed regarding cartilage degradation in OA may therefore not be lead us to conclude that adiponectin could be accountable for degradation of the cartilage. Rather, increased levels of adiponectin may be a secondary phenomenon to the late stage of OA, which could be deemed an indication of generalised to whole stages. Koskinen and colleagues’ severity. Another explanation could be that increased study should be evaluated in light of this knowledge [1]. I read with great interest Koskinen and colleagues’ levels of adiponectin may serve as a protective response to the catabolic process in OA e current under stand- article about the role of adiponectin on cartilage degra- ing of cytokines and growth factors has been shown da tion in OA e authors showed that plasma incapable of determining a single factor that could be responsible for all chondrocyte responses [3]. adiponectin levels and adiponectin released from OA cartilage were higher in patients with the radiographically Another point to be raised in this study would be the ey suggested that adiponectin is e? ect of adiponectin on OA cartilage and primary more severe OA associated with cartilage destruction in OA [1]. Making chondrocytes in vitro. Koskinen and colleagues reported an extrapolation based on a cross-sectional study in that adipone