Ghiassi-Nejad Zahra, Friedman Scott L
Division of Liver Diseases, Box 1123, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, NY 10029, USA.
Expert Rev Gastroenterol Hepatol. 2008 Dec;2(6):803-16. doi: 10.1586/17474124.2.6.803.
Sustained progress in defining the molecular pathophysiology of hepatic fibrosis has led to a comprehensive framework for developing antifibrotic therapies. Indeed, the single greatest limitation in bringing new drugs to the clinical setting is a lack of clarity regarding clinical trial and treatment end points, not a lack of promising agents. A range of treatments, including those developed for other indications, as well as those specifically developed for hepatic fibrosis, are nearing or in clinical trials. Most are focused on attacking features of either hepatic injury and/or activated stellate cells and myofibroblasts, which are the primary sources of extracellular matrix (scar) proteins. Thus, features of injury and stellate cell activation provide a useful template for classifying these emerging agents and point to a new class of therapies for patients with fibrosing liver disease.
在明确肝纤维化分子病理生理学方面取得的持续进展，已形成了一个用于开发抗纤维化疗法的全面框架。事实上，将新药推向临床应用的最大限制在于缺乏关于临床试验和治疗终点的明确认识，而非缺乏有前景的药物。一系列治疗方法，包括那些针对其他适应症开发的以及专门为肝纤维化开发的，正接近或已进入临床试验阶段。大多数治疗方法聚焦于攻击肝损伤和/或活化的星状细胞及肌成纤维细胞的特征，这些细胞是细胞外基质（瘢痕）蛋白的主要来源。因此，损伤和星状细胞活化的特征为分类这些新兴药物提供了有用的模板，并为纤维化肝病患者指明了一类新的治疗方法。
