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Necroptosis and Inflammation

Kim Newton1, Gerard Manning2

  • 1Physiological Chemistry Department, Genentech, Inc., South San Francisco, California 94080;

Annual Review of Biochemistry
|February 12, 2016
PubMed

Insights

Necroptosis, a regulated cell death, triggers immune responses when caspase-8 is inhibited. Targeting RIPK1 or RIPK3 kinases may offer therapeutic benefits for inflammatory diseases.

Area of Science:

  • Cellular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Necroptosis is a regulated form of necrosis.
  • It involves cell rupture and release of intracellular components, initiating innate immune responses.
  • Triggers include TLR agonists, TNF, viral infections, or TCR activation when caspase-8 is inhibited.

Purpose of the Study:

  • To explore the role of RIPK1 and RIPK3 kinases in necroptosis.
  • To investigate the therapeutic potential of inhibiting these kinases.

Main Methods:

  • Analysis of necroptosis signaling pathways.
  • Evaluation of RIPK3 deficiency and RIPK1 inhibition in disease models.

Main Results:

  • Necroptosis signaling requires RIPK3 and MLKL, modulated by RIPK1.
  • RIPK3 deficiency or RIPK1 inhibition confers resistance in animal models.
  • Inflammation from necroptosis contributes to tissue damage.

Conclusions:

  • RIPK1 and RIPK3 are key regulators of necroptosis and inflammation.
  • Inhibitors of RIPK1 or RIPK3 show therapeutic potential for inflammatory conditions.
  • These kinases may regulate cell death programs beyond necroptosis.
Keywords:
MLKLRIPK1RIPK3

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