Laboratory of Immunorheumatology and Tissue Regeneration/RAMSES, Rizzoli Orthopaedic Institute, Bologna, Italy.
Ther Adv Chronic Dis. 2013 Jan;4(1):23-43. doi: 10.1177/2040622312462734.
This review focuses on the new perspectives which can provide insight into the crucial pathways that drive cartilage-bone physiopathology. In particular, we discuss the critical signaling and effector molecules that can activate cellular and molecular processes in both cartilage and bone cells and which may be relevant in cross talk among joint compartments: growth factors (bone morphogenetic proteins and transforming growth factor), hypoxia-related factors, cell-matrix interactions [discoidin domain receptor 2 (DDR2) and syndecan 4], signaling molecules [WNT, Hedgehog (Hh)]. With the continuous progression of our knowledge on the molecular pathways involved in cartilage and bone changes in osteoarthritis (OA), an increasing number of potentially effective candidates for OA therapy are already under scrutiny in clinical trials to ascertain their possible safe use in an attempt to identify molecules active in slowing or halting OA progression and reducing joint pain. We then review the principal molecules currently under clinical investigation.
这篇综述重点介绍了一些新视角，这些新视角可以深入了解驱动软骨-骨病理生理学的关键途径。特别是，我们讨论了关键的信号和效应分子，这些分子可以激活软骨细胞和骨细胞中的细胞和分子过程，并且可能与关节间隙之间的串扰有关：生长因子（骨形态发生蛋白和转化生长因子）、缺氧相关因子、细胞-基质相互作用[盘状结构域受体 2 (DDR2)和 syndecan 4]、信号分子[WNT、Hedgehog (Hh)]。随着我们对骨关节炎 (OA) 中软骨和骨变化涉及的分子途径的不断深入了解，越来越多的潜在有效的 OA 治疗候选药物已经在临床试验中受到审查，以确定它们在尝试识别可减缓或阻止 OA 进展和减轻关节疼痛的有效分子时的可能安全使用。然后，我们回顾了目前正在临床研究的主要分子。
