Necroptosis: a regulated inflammatory mode of cell death

J Neuroinflammation. 2018 Jul 6;15(1):199. doi: 10.1186/s12974-018-1235-0.

Yogesh K Dhuriya ¹ ², Divakar Sharma ³ ⁴

Affiliations

1 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.
2 Academy of Scientific and Innovative Research (AcSIR) Lucknow Campus, Lucknow, India.
3 Department of Biochemistry, National JALMA Institute for Leprosy and Other Mycobacterial Diseases, Tajganj, Agra, India. [email protected].
4 Interdisciplinary Biotechnology Unit, Aligarh Muslim University, Aligarh, 202002, India. [email protected].

PMID: 29980212 DOI: 10.1186/s12974-018-1235-0

Abstract

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.

Keywords

Inflammation; MLKL; Necroptosis; Neurodegenerative disease; RIPK3.

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