Hepatic inflammation and progressive liver fibrosis in chronic liver disease
Hepatic inflammation and progressive liver fibrosis in chronic liver disease
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DOI：
10.3748/wjg.v20.i10.2515
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发表时间：
2014-03-14
影响因子：
4.3
通讯作者：
Czaja, Albert J.
中科院分区：
文献类型：
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作者：
Czaja, Albert J.
慢性肝炎导致肝纤维化，目前的免疫抑制、抗炎和抗病毒治疗可以削弱这一驱动因素。在57%-79%的患者中，通过传统的治疗方案，肝纤维化可以逆转、稳定或预防，主要是通过抗炎作用。然而，回应通常是不完整和不一致的。与肝脏炎症相关的纤维化机制已被阐明，抗纤维化药物有望作为辅助治疗改善结果。丙型肝炎病毒和免疫介导的反应可以通过增加肝细胞内的氧化应激来激活肝星状细胞。血管紧张素可由活化的肝星状细胞合成，并促进活性氧的产生。在初步的人体研究中，抗氧化剂(N-乙酰半胱氨酸、S-腺苷-L-蛋氨酸和维生素E)和血管紧张素抑制剂(Losartin)具有抗纤维化作用，它们可能会作为补充疗法出现。抗纤维化药物预示着慢性肝病补充治疗的新时代。(C)2014年白石登出版集团有限公司。版权所有。
Chronic liver inflammation drives hepatic fibrosis, and current immunosuppressive, anti-inflammatory, and anti-viral therapies can weaken this driver. Hepatic fibrosis is reversed, stabilized, or prevented in 57%-79% of patients by conventional treatment regimens, mainly by their anti-inflammatory actions. Responses, however, are commonly incomplete and inconsistently achieved. The fibrotic mechanisms associated with liver inflammation have been clarified, and anti-fibrotic agents promise to improve outcomes as adjunctive therapies. Hepatitis C virus and immune-mediated responses can activate hepatic stellate cells by increasing oxidative stress within hepatocytes. Angiotensin can be synthesized by activated hepatic stellate cells and promote the production of reactive oxygen species. Anti-oxidants (N acetylcysteine, S-adenosyl-L-methionine, and vitamin E) and angiotensin inhibitors (losartin) have had anti-fibrotic actions in preliminary human studies, and they may emerge as supplemental therapies. Anti-fibrotic agents presage a new era of supplemental treatment for chronic liver disease. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.