April 1, 2002 | Axel M. Gressner, Ralf Weiskirchen, Katja Breitkopf, Steven Dooley
The article discusses the roles of transforming growth factor beta (TGF-β) in hepatic fibrosis. TGF-β has both profibrogenic and anti-inflammatory effects, maintaining tissue homeostasis. Its aberrant expression is involved in various liver diseases. TGF-β promotes hepatic stellate cell (HSC) transdifferentiation into myofibroblasts, stimulates ECM production, and induces apoptosis in hepatocytes. The activation of HSC by TGF-β is a key mechanism in liver fibrosis. TGF-β signaling involves the activation of Smad proteins, which mediate transcriptional responses. The article also explores the potential of circulating TGF-β as a diagnostic tool and therapeutic targets for antifibrotic strategies, including抗氧化剂、特定药物、草药化合物、中和抗体、TGF-β结合蛋白、拮抗性细胞因子、凋亡抑制剂、以及基因疗法。未来的研究将集中在更精确地干预TGF-β的过度或不足,以恢复其在肝脏疾病中的平衡作用。The article discusses the roles of transforming growth factor beta (TGF-β) in hepatic fibrosis. TGF-β has both profibrogenic and anti-inflammatory effects, maintaining tissue homeostasis. Its aberrant expression is involved in various liver diseases. TGF-β promotes hepatic stellate cell (HSC) transdifferentiation into myofibroblasts, stimulates ECM production, and induces apoptosis in hepatocytes. The activation of HSC by TGF-β is a key mechanism in liver fibrosis. TGF-β signaling involves the activation of Smad proteins, which mediate transcriptional responses. The article also explores the potential of circulating TGF-β as a diagnostic tool and therapeutic targets for antifibrotic strategies, including抗氧化剂、特定药物、草药化合物、中和抗体、TGF-β结合蛋白、拮抗性细胞因子、凋亡抑制剂、以及基因疗法。未来的研究将集中在更精确地干预TGF-β的过度或不足,以恢复其在肝脏疾病中的平衡作用。