Review

Cellular and Molecular Life Sciences

, Volume 67, Issue 19, pp 3241-3253

First online:

Going up in flames: necrotic cell injury and inflammatory diseases

  • Sreerupa ChallaAffiliated withDepartment of Pathology, Immunology and Virology Program Diabetes and Endocrinology Center, University of Massachusetts Medical School
  • , Francis Ka-Ming ChanAffiliated withDepartment of Pathology, Immunology and Virology Program Diabetes and Endocrinology Center, University of Massachusetts Medical SchoolDepartment of Pathology, University of Massachusetts Medical School Email author 

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Abstract

Recent evidence indicates that cell death can be induced through multiple mechanisms. Strikingly, the same death signal can often induce apoptotic as well as non-apoptotic cell death. For instance, inhibition of caspases often converts an apoptotic stimulus to one that causes necrosis. Because a dedicated molecular circuitry distinct from that controlling apoptosis is required for necrotic cell injury, terms such as “programmed necrosis” or “necroptosis” have been used to distinguish stimulus-dependent necrosis from those induced by non-specific traumas (e.g., heat shock) or secondary necrosis induced as a consequence of apoptosis. In several experimental models, programmed necrosis/necroptosis has been shown to be a crucial control point for pathogen- or injury-induced inflammation. In this review, we will discuss the molecular mechanisms that regulate programmed necrosis/necroptosis and its biological significance in pathogen infections, drug-induced cell injury, and trauma-induced tissue damage.

Keywords

RIP1 RIP3 Programmed necrosis Inflammation TNF