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Sreerupa Challa Francis Ka-Ming Chan 《Cellular and molecular life sciences : CMLS》2010,67(19):3241-3253
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. 相似文献
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