Pathophysiology of decompensated cirrhosis: Portal hypertension, circulatory dysfunction, inflammation, metabolism and mitochondrial dysfunction.
Pathophysiology of decompensated cirrhosis: Portal hypertension, circulatory dysfunction, inflammation, metabolism and mitochondrial dysfunction.
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DOI：
10.1016/j.jhep.2021.01.002
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发表时间：
2021-07
影响因子：
25.7
通讯作者：
Bernardi, Mauro
中科院分区：
文献类型：
--
作者：
Engelmann, Cornelius;Claria, Joan;Szabo, Gyongyi;Bosch, Jaume;Bernardi, Mauro
关键词：
急性失代偿性肝硬化患者预后不良，经常进展为急性-慢性肝功能衰竭，其特征为肝和肝外器官衰竭。失代偿和疾病进展中涉及的病理机制仍然没有很好地理解，并且由于不存在特定的疾病修饰治疗，因此确定新的治疗靶点的研究至关重要。这篇综述融合了导致组织损伤和肝外器官衰竭的疾病机制的最新知识-如全身炎症，线粒体功能障碍，氧化应激和代谢变化-并将这些与急性失代偿的经典范例结合起来，形成一个单一的范例。通过对病理机制的详细分析，我们确定了未来研究的领域。迫切需要打破恶性循环的新型疾病修饰策略来改善患者的预后。
Patients with acutely decompensated cirrhosis have a dismal prognosis and frequently progress to acuteon-chronic liver failure, which is characterised by hepatic and extrahepatic organ failure(s). The pathomechanisms involved in decompensation and disease progression are still not well understood, and as specific disease-modifying treatments do not exist, research to identify novel therapeutic targets is of the utmost importance. This review amalgamates the latest knowledge on disease mechanisms that lead to tissue injury and extrahepatic organ failure – such as systemic inflammation, mitochondrial dysfunction, oxidative stress and metabolic changes – and marries these with the classical paradigms of acute decompensation to form a single paradigm. With this detailed breakdown of pathomechanisms, we identify areas for future research. Novel disease-modifying strategies that break the vicious cycle are urgently required to improve patient outcomes.
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影响因子：
24.5
作者：
Bernardi, Mauro;Angeli, Paolo;Arroyo, Vicente
通讯作者：
Arroyo, Vicente
影响因子：
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作者：
Berzigotti A
通讯作者：
Berzigotti A
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作者：
Bellis, L;Berzigotti, A;Rodés, J
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Rodés, J
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Bellot, Pablo;Carlos Garcia-Pagan, Juan;Bosch, Jaime
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作者：
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