Going up in flames: necrotic cell injury and inflammatory diseases

作者：Challa Sreerupa; Chan Francis Ka Ming^*

来源：Cellular and Molecular Life Sciences, 2010, 67(19): 3241-3253.

DOI：10.1007/s00018-010-0413-8

• RIP1
• RIP3
• Programmed necrosis
• Inflammation
• TNF

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.

• 出版日期2010-10