Developmental Toxicology Laboratory, Systems Toxicology and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan; 31, Mahatma Gandhi Marg, Lucknow, 226001, India.
Academy of Scientific and Innovative Research (AcSIR) Lucknow Campus, Lucknow, India.
J Neuroinflammation. 2018 Jul 6;15(1):199. doi: 10.1186/s12974-018-1235-0.
Programmed cell death has a vital role in embryonic development and tissue homeostasis. Necroptosis is an alternative mode of regulated cell death mimicking features of apoptosis and necrosis. Necroptosis requires protein RIPK3 (previously well recognized as regulator of inflammation, cell survival, and disease) and its substrate MLKL, the crucial players of this pathway. Necroptosis is induced by toll-like receptor, death receptor, interferon, and some other mediators. Shreds of evidence based on a mouse model reveals that deregulation of necroptosis has been found to be associated with pathological conditions like cancer, neurodegenerative diseases, and inflammatory diseases. In this timeline article, we are discussing the molecular mechanisms of necroptosis and its relevance to diseases.
程序性细胞死亡在胚胎发育和组织稳态中起着至关重要的作用。细胞坏死是一种受调控的细胞死亡方式,其特征类似于细胞凋亡和细胞坏死。细胞坏死需要蛋白 RIPK3(以前被认为是炎症、细胞存活和疾病的调节剂)及其底物 MLKL,这是该途径的关键参与者。细胞坏死由 Toll 样受体、死亡受体、干扰素和其他一些介质诱导。基于小鼠模型的大量证据表明,细胞坏死的失调与癌症、神经退行性疾病和炎症性疾病等病理状况有关。在这篇时间线文章中,我们讨论了细胞坏死的分子机制及其与疾病的相关性。