Going up in flames: necrotic cell injury and inflammatory diseases |
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Authors: | Sreerupa Challa Francis Ka-Ming Chan |
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Institution: | (1) Department of Pathology, Immunology and Virology Program Diabetes and Endocrinology Center, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA;(2) Department of Pathology, University of Massachusetts Medical School, Room S2-125, Worcester, MA 01655, USA; |
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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. |
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