Liver fibrosis and cirrhosis resulting from long-standing liver damage represents a major health care burden worldwide. To date, there is no anti-fibrogenic agent available, making liver transplantation the only curative treatment for decompensated cirrhotic liver disease. Liver fibrosis can result from different underlying chronic liver disease, such as chronic viral infection, excessive alcohol consumption, fatty liver disease or autoimmune liver diseases. It is becoming increasingly recognised that as a result from different pathogenic mechanisms liver fibrosis must be considered as many different diseases for which individual treatment strategies need to be developed. Moreover, the pathogenic changes of both liver architecture and vascularisation in cirrhotic livers, as well as the lack of “true-to-life” in vitro models have impeded the development of an effective anti-fibrogenic drug. Thus, in order to identify an efficient anti-fibrogenic compound, novel in-vitro models mimicking the interplay between pro-fibrogenic cell populations, immune cells and, importantly, the extracellular matrix need to be developed.

长期肝损害导致的肝纤维化和肝硬化代表了全球主要的医疗保健负担。迄今为止，尚无抗纤维化剂，使肝移植成为失代偿性肝硬化肝病的唯一治疗方法。肝纤维化可以由不同的潜在慢性肝脏疾病引起，例如慢性病毒感染，过量饮酒，脂肪肝疾病或自身免疫性肝病。越来越多的人认识到，由于不同的致病机制，肝纤维化必须被视为许多不同的疾病，需要针对这些疾病制定单独的治疗策略。此外，肝硬化肝脏的肝脏结构和血管形成的致病性变化，以及缺乏“逼真的”体外模型阻碍了有效抗纤维化药物的开发。因此，为了鉴定有效的抗成纤维化合物，需要开发新的体外模型，其模拟成纤维细胞群，免疫细胞以及重要的是细胞外基质之间的相互作用。