Necroptosis is a noncaspase-dependent and precisely regulated mechanism of cell death. Necroptosis is mainly initiated by members of the tumor necrosis factor receptor (TNFR) and Toll-like receptor (TLR) families, interferon, intracellular RNA and DNA sensors and other mediators. Subsequently, the protein kinase RIPK1 (receptor-interacting protein kinase 1) and RIPK3 interact with the receptor protein, which transduces death signals and further recruits and phosphorylates MLKL (mixed lineage kinase domain-like protein). MLKL serves as the initiator of cell death and eventually induces necroptosis. It was found that necroptosis is not only involved in the physiological regulation but also in the occurrence, development and prognosis of some necrotic diseases, especially infectious diseases. Intervention in the necroptosis signaling pathway is helpful for removing pathogens, inhibiting the development of lesions, and promoting the remodeling of tissue. In-depth study of the molecular regulation mechanism of necroptosis and its relationship with the pathogenesis of infectious diseases will help to provide new ideas and directions for research of the pathological mechanisms and clinical prevention of infectious diseases.

中文翻译：

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坏死病及其在传染病中的作用。

坏死病是一种非胱天蛋白酶依赖性细胞死亡的精确调控机制。坏死病主要由肿瘤坏死因子受体（TNFR）和Toll样受体（TLR）家族成员，干扰素，细胞内RNA和DNA传感器及其他介质引发。随后，蛋白激酶RIPK1（与受体相互作用的蛋白激酶1）和RIPK3与受体蛋白相互作用，该受体蛋白转导死亡信号并进一步募集并磷酸化MLKL（混合的谱系激酶结构域样蛋白）。MLKL充当细胞死亡的引发剂，并最终诱导坏死性坏死。发现坏死性坏死不仅涉及生理调节，而且还涉及某些坏死性疾病，特别是传染性疾病的发生，发展和预后。坏死病信号通路的干预有助于去除病原体，抑制病变的发展并促进组织的重塑。深入研究坏死病的分子调控机制及其与传染病发病机制的关系，将为研究传染病的病理机制和临床预防提供新的思路和方向。