Trippel S B
Orthopaedic Research Laboratories, Massachusetts General Hospital, Boston 02114, USA.
J Rheumatol Suppl. 1995 Feb;43:129-32.
Polypeptide growth factors play a major role in the regulation of cell behavior, including that of articular chondrocytes. Among the most influential of these factors identified for articular cartilage are insulin like growth factor I (IGF-I), basic fibroblast growth factor (bFGF), and transforming growth factor beta (TGF beta). IGF-I stimulates articular chondrocyte matrix synthetic and mitotic activity and inhibits chondrocyte mediated matrix catabolism. The role of bFGF as a potent mitogen for articular chondrocytes is well established. In contrast, this factor appears to play a complex role in matrix synthesis and degradation, promoting both anabolic and catabolic functions. Both IGF-I and bFGF have been shown to augment articular cartilage repair in vivo. TGF beta is particularly dependent upon the context in which it acts, eliciting seemingly opposite effects under different experimental conditions. These and other factors interact to modulate their respective actions, creating effector cascades and feedback loops of intercellular and intracellular events that control articular chondrocyte functions. Elucidation of the actions and interactions of these factors may be expected to clarify the etiopathogenesis of osteoarthritis and possibly offer novel methods for its treatment.
多肽生长因子在调节细胞行为（包括关节软骨细胞行为）中起主要作用。在已确定的对关节软骨最具影响力的这些因子中，有胰岛素样生长因子I（IGF-I）、碱性成纤维细胞生长因子（bFGF）和转化生长因子β（TGFβ）。IGF-I刺激关节软骨细胞基质合成和有丝分裂活性，并抑制软骨细胞介导的基质分解代谢。bFGF作为关节软骨细胞的一种有效促有丝分裂原，其作用已得到充分证实。相比之下，该因子在基质合成和降解中似乎发挥着复杂的作用，既促进合成代谢功能，也促进分解代谢功能。IGF-I和bFGF在体内均已显示可增强关节软骨修复。TGFβ尤其依赖于其作用的环境，在不同实验条件下会引发看似相反的效应。这些因子与其他因子相互作用以调节各自的作用，形成控制关节软骨细胞功能的细胞间和细胞内事件的效应器级联反应和反馈回路。对这些因子的作用和相互作用的阐明有望澄清骨关节炎的发病机制，并可能提供新的治疗方法。
