Necroptosis: a regulated inflammatory mode of cell death

By Y. K. Dhuriya, D. Sharma. Journal of Neuroinflammation, 2018

609 citations recorded by the source corpus.

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.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/6ba3c1223d6146776e473dbd5c894dc6e1755d2c

Citations in the corpus

• Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes (2020, neutral): “Necroptosis is executed by RIPK3-mediated MLKL oligomerization (Dhuriya and Sharma, 2018; Giampietri et al., 2014; Murphy et al., 2013).”