PerspectiveCell Biology

RIPK3 Takes Another Deadly Turn

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Science  21 Mar 2014:
Vol. 343, Issue 6177, pp. 1322-1323
DOI: 10.1126/science.1252526

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Programmed necrosis, or necroptosis, is a form of cell death with important roles in many inflammatory conditions, such as innate antiviral responses and atherosclerosis. It is a messy process, characterized by cell swelling and eventual rupture that releases contents into the surroundings, triggering inflammation. Initially considered an unregulated response to nonspecific stress, necroptosis is now understood to be controlled by signaling pathways that intersect with the regulation of apoptosis, a well-characterized programmed cell death mechanism. By contrast, apoptosis is relatively neat and does not trigger an inflammatory response. Determining how a cell succumbs to one form of cell death and not the other may guide the development of therapeutic strategies for acute and chronic inflammatory diseases. On page 1357 of this issue, Newton et al. (1) elucidate how the two cell death mechanisms intersect, and discover that disrupting one process leads to a surprising consequence—death by the other.