https://scholars.lib.ntu.edu.tw/handle/123456789/551121
標題: | Molecular mechanism and treatment of viral hepatitis-related liver fibrosis | 作者: | TUNG-HUNG SU JIA-HORNG KAO CHUN-JEN LIU |
公開日期: | 2014 | 出版社: | MDPI AG | 卷: | 15 | 期: | 6 | 起(迄)頁: | 10578-10604 | 來源出版物: | International Journal of Molecular Sciences | 摘要: | Hepatic fibrosis is a wound-healing response to various chronic stimuli, including viral hepatitis B or C infection. Activated myofibroblasts, predominantly derived from the hepatic stellate cells (HSCs), regulate the balance between matrix metalloproteinases and their tissue inhibitors to maintain extracellular matrix homeostasis. Transforming growth factor-β and platelet-derived growth factor are classic profibrogenic signals that activate HSC proliferation. In addition, proinflammatory cytokines and chemokines coordinate macrophages, T cells, NK/NKT cells, and liver sinusoidal endothelial cells in complex fibrogenic and regression processes. In addition, fibrogenesis involves angiogenesis, metabolic reprogramming, autophagy, microRNA, and epigenetic regulations. Hepatic inflammation is the driving force behind liver fibrosis; however, host single nucleotide polymorphisms and viral factors, including the genotype, viral load, viral mutation, and viral proteins, have been associated with fibrosis progression. Eliminating the underlying etiology is the most crucial antifibrotic therapy. Growing evidence has indicated that persistent viral suppression with antiviral therapy can result in fibrosis regression, reduced liver disease progression, decreased hepatocellular carcinoma, and improved chances of survival. Preclinical studies and clinical trials are currently examining several investigational agents that target key fibrogenic pathways; the results are promising and shed light on this debilitating illness. ? 2014 by the authors; licensee MDPI, Basel, Switzerland. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84902330457&doi=10.3390%2fijms150610578&partnerID=40&md5=19894ea3c0404ee41c099c52439f0584 https://scholars.lib.ntu.edu.tw/handle/123456789/551121 |
ISSN: | 1661-6596 | DOI: | 10.3390/ijms150610578 | SDG/關鍵字: | adefovir dipivoxil; angiotensin receptor antagonist; atorvastatin; dipeptidyl carboxypeptidase inhibitor; entecavir; fresolimumab; host factor; immunomodulating agent; lamivudine; microRNA; nintedanib; pioglitazone; pirfenidone; platelet derived growth factor; prm 151; sar 156597; simtuzumab; sorafenib; statin (protein); stx 100; telbivudine; tenofovir; tralokinumab; transforming growth factor beta; unclassified drug; antivirus agent; microRNA; protein kinase inhibitor; angiogenesis; antiviral therapy; autophagy; cell proliferation; disease course; endothelium cell; epigenetics; fibrogenesis; fibrosing alveolitis; focal glomerulosclerosis; gene mutation; genotype; hepatitis B; hepatitis C; human; inflammation; liver cell carcinoma; liver cirrhosis; liver fibrosis; macrophage; membrane vesicle; metabolic regulation; myelofibrosis; myofibroblast; natural killer cell; natural killer T cell; nonhuman; phase 2 clinical trial (topic); phase 3 clinical trial (topic); polarization; remission; review; single nucleotide polymorphism; stellate cell; T lymphocyte; virus hepatitis; virus load; CD4+ T lymphocyte; complication; cytology; Hepatitis, Viral, Human; immunology; liver cirrhosis; metabolism; Angiotensin-Converting Enzyme Inhibitors; Antiviral Agents; CD4-Positive T-Lymphocytes; Hepatic Stellate Cells; Hepatitis, Viral, Human; Humans; Liver Cirrhosis; MicroRNAs; Protein Kinase Inhibitors |
顯示於: | 醫學系 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。