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


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

  • 20532807

Electronic International Standard Serial Number (EISSN)

  • 1420-9071

Digital Object Identifier (DOI)

  • 10.1007/s00018-010-0413-8


  • eng

Conference Location

  • Switzerland