Necrosis, a type of unwanted and passive cell demise, usually occurs under the excessive external stress and is considered to be unregulated. However, under some special conditions such as caspase inhibition, necrosis is regulable in a well-orchestrated way. The term 'regulated necrosis' has been proposed to describe such programed necrosis. Recently, several forms of necrosis, including necroptosis, pyroptosis, ferroptosis, parthanatos, oxytosis, NETosis, and Na+/K+-ATPase-mediated necrosis, have been identified, and some crucial regulators governing regulated necrosis have also been discovered. Mixed lineage kinase domain-like pseudokinase (MLKL), a core regulator in necroptosis, acts as an executioner in response to ligands of death receptor family. Its activation requires the receptor-interacting protein kinases, RIP1 and RIP3. However, MLKL is only involved in necroptosis, i.e. MLKL is dispensable for necrosis. Therefore, this review is aimed at summarizing the molecular mechanisms of MLKL-dependent and MLKL-independent necrosis.

中文翻译：

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MLKL 依赖性和 MLKL 非依赖性坏死的分子机制。

坏死是一种不需要的和被动的细胞死亡，通常发生在过度的外部压力下，被认为是不受监管的。然而，在某些特殊条件下，如半胱天冬酶抑制，坏死是可以通过精心安排的方式进行调节的。已经提出术语“调节性坏死”来描述这种程序性坏死。最近，已经确定了几种形式的坏死，包括坏死性凋亡、焦亡、铁死亡、parthanatos、催产素、NETosis 和 Na+/K+-ATP 酶介导的坏死，并且还发现了一些控制调节性坏死的关键调节因子。混合谱系激酶结构域样假激酶 (MLK​​L) 是坏死性凋亡的核心调节因子，在响应死亡受体家族的配体时充当刽子手。它的激活需要与受体相互作用的蛋白激酶 RIP1 和 RIP3。然而，MLKL只参与坏死性凋亡，即MLKL对于坏死是可有可无的。因此，本综述旨在总结 MLKL 依赖性和 MLKL 非依赖性坏死的分子机制。