Acute and chronic liver injury results in hepatocyte death and turnover. If injury becomes chronic, the continuous cell death and turnover leads to chronic inflammation, fibrosis and ultimately cirrhosis and hepatocellular carcinoma. Controlling liver cell death both in acute injury, to rescue the liver from acute liver failure, and in chronic injury, to curb secondary inflammation and fibrosis, is of paramount importance as a therapeutic strategy. Both apoptosis and necrosis occur in the liver, but the occurrence of necroptosis in the liver and its contribution to liver disease is controversial. Necroptosis is a form of regulated necrosis which occurs in certain cell types when caspases (+/-cIAPs) are inhibited through the RIPK1-RIPK3 activation of MLKL. The occurrence of necroptosis in the liver has recently been examined in multiple liver injury models with conflicting results. The aim of this review is to summarize the published data with an emphasis on the controversies and remaining questions in the field.

中文翻译：

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问题和争议：坏死病在肝病中的作用。

急性和慢性肝损伤导致肝细胞死亡和更新。如果损伤变为慢性，则连续的细胞死亡和更新会导致慢性炎症，纤维化，最终导致肝硬化和肝细胞癌。作为治疗策略，控制急性损伤中的肝细胞死亡以挽救急性肝衰竭，以及控制慢性损伤中的继发性炎症和纤维化都是至关重要的。肝中均发生凋亡和坏死，但是在肝脏中发生坏死性皮肤病及其对肝脏疾病的贡献是有争议的。坏死性坏死是一种调节性坏死的形式，当通过MLKL的RIPK1-RIPK3激活抑制胱天蛋白酶（+/- cIAPs）时，在某些细胞类型中会发生。最近已经在多种肝损伤模型中检查了肝坏死病的发生，但结果相互矛盾。本文的目的是总结已发表的数据，重点是该领域的争议和尚存的问题。