Necroptosis: Mechanisms and Relevance to Disease Review uri icon


MeSH Major

  • Apoptosis
  • Disease
  • Necrosis
  • Receptor-Interacting Protein Serine-Threonine Kinases


  • 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.

publication date

  • January 24, 2017



  • Review



  • eng

Digital Object Identifier (DOI)

  • 10.1146/annurev-pathol-052016-100247

PubMed ID

  • 27959630

Additional Document Info

start page

  • 103

end page

  • 130


  • 12