Necroptosis: Mechanisms and Relevance to Disease

By L. Galluzzi, Oliver Kepp, F. Chan, Guido Kroemer. Annual Review of Pathology, 2016

648 citations recorded by the source corpus.

Necroptosis is a form of regulated cell death that critically depends on receptor-interacting serine-threonine kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) and generally manifests with morphological features of necrosis. The molecular mechanisms that underlie distinct instances of necroptosis have just begun to emerge. Nonetheless, it has already been shown that necroptosis contributes to cellular demise in various pathophysiological conditions, including viral infection, acute kidney injury, and cardiac ischemia/reperfusion. Moreover, human tumors appear to obtain an advantage from the downregulation of key components of the molecular machinery for necroptosis. Although such an advantage may stem from an increased resistance to adverse microenvironmental conditions, accumulating evidence indicates that necroptosis-deficient cancer cells are poorly immunogenic and hence escape natural and therapy-elicited immunosurveillance. Here, we discuss the molecular mechanisms and relevance to disease of necroptosis.

Subfields: Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d878caa4bdb8361393f895d74d65427b8c498ea8

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Citations in the corpus

Mitochondrial metabolism and cancer (2017, background): “Discussing the regulation of apoptotic and necrotic RCD by mitochondria in details goes beyond the scope of the present review [167, 168].”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “Thus, RCD stands out as a major therapeutic target for the management of multiple human disorders [1, 2, 649, 1043].”