Going up in flames: necrotic cell injury and inflammatory diseases.

Journal Article (Journal Article;Review)

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.

Full Text

Duke Authors

Cited Authors

  • Challa, S; Chan, FK-M

Published Date

  • October 2010

Published In

Volume / Issue

  • 67 / 19

Start / End Page

  • 3241 - 3253

PubMed ID

  • 20532807

Pubmed Central ID

  • PMC3051829

Electronic International Standard Serial Number (EISSN)

  • 1420-9071

Digital Object Identifier (DOI)

  • 10.1007/s00018-010-0413-8

Language

  • eng

Conference Location

  • Switzerland