RESUMO
Currently, liver fibrosis and its complications are regarded as critical health problems. With the studies showing the reversible nature of liver fibrogenesis, scientists have focused on understanding the underlying mechanism of this condition in order to develop new therapeutic strategies. Although hepatic stellate cells are known as the primary cells responsible for liver fibrogenesis, studies have shown contributing roles for other cells, pathways, and molecules in the development of fibrosis depending on the etiology of liver fibrosis. Hence, interventions could be directed in the proper way for each type of liver diseases to better address this complication. There are two main approaches in clinical reversion of liver fibrosis; eliminating the underlying insult and targeting the fibrosis process, which have variable clinical importance in the treatment of this disease. In this review, we present recent concepts in molecular pathways of liver fibrosis reversibility and their clinical implications
RESUMO
Liver fibrosis is a potentially reversible response to hepatic insults, triggered by different chronic diseases most importantly viral hepatitis, alcoholic, and nonalcoholic fatty liver disease. In the course of the chronic liver disease, hepatic fibrogenesis may develop, which is attributed to various types of cells, molecules, and pathways. Activated hepatic stellate cell [HSC], the primary source of extracellular matrix [ECM], is fundamental in pathophysiology of fibrogenesis, and thus is the most attractable target for reversing liver fibrosis. Although, liver biopsy has long been considered as the gold standard for diagnosis and staging of hepatic fibrosis, assessing progression and regression by biopsy is hampered by its limitations. We provide recent views on noninvasive approaches including serum biomarkers and radiologic techniques