[The molecular mechanism of necroptosis]

Yi Chuan. 2014 Jun;36(6):519-24. doi: 10.3724/SP.J.1005.2014.0519.
[Article in Chinese]

Abstract

Programmed necrosis called necroptosis, is different from traditional necrosis and apoptosis, it has attracted considerable attention over the last few years. Necroptosis can be initiated through many factors such as tumor necrosis factor receptor (TNFR) or pattern recognition receptor (PRR), and receptor-interacting protein (RIP) 1 and 3 are two key proteins during the process. A lot of molecules have been characterized as modulators and effectors of necroptosis, including poly(ADP-ribose) polymerase (PARP-1), reactive oxygen species (ROS), Ca(2+), which can destruct mitochondria or other organelles and induce cell dead through caspase-independent pathway. Then, damage-associated molecular pattern (DAMP) molecules were released from necroptosis cells, recognized and internalized by phagocytes. Here, we briefly discuss the initiation and execution of necroptosis and the clearance of death cells.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis*
  • Humans
  • Necrosis*
  • Poly(ADP-ribose) Polymerases / genetics
  • Poly(ADP-ribose) Polymerases / metabolism
  • Receptors, Tumor Necrosis Factor / genetics
  • Receptors, Tumor Necrosis Factor / metabolism
  • Signal Transduction*
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Poly(ADP-ribose) Polymerases