Apoptosis

Definition

Apoptosis is a mechanism of programmed cell death and is essential for development and homeostasis. Cell stress stimulates pro-apoptotic signalling pathways that activate caspase proteases and cause mitochondrial dysfunction. Apoptotic cells undergo characteristic changes in cell morphology, including cell rounding, plasma membrane blebbing and nuclear fragmentation.

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News and Comment

  • News and Views |

    The cytokine tumour necrosis factor (TNF) and the toll-like receptors (TLRs) coordinate immune responses by activating inflammatory transcriptional programs, but these signals can also trigger cell death. Recent studies identify the MAP kinase substrate MK2 as a key player in determining whether cells live or die in response to TNF and TLR signalling.

    • Andrew Oberst
    Nature Cell Biology 19, 1150–1152
  • News and Views |

    Cancer treatments often focus on killing tumour cells through apoptosis, which is thought to typically require mitochondrial outer membrane permeabilization (MOMP) and subsequent caspase activation. A study now shows that MOMP can trigger TNF-dependent, but caspase-independent cell death, suggesting a different approach to improve cancer therapy.

    • Brent E. Fitzwalter
    •  & Andrew Thorburn
    Nature Cell Biology 19, 1014–1015
  • News and Views |

    During injury, mitogenic signals from apoptotic cells may compensate for cell loss by promoting organ homeostasis and regeneration. A distinct type of early apoptotic extracellular vesicle with specific mitogenic activity has been identified. The detection of these vesicles in damaged mouse glomeruli highlights their possible role in response to renal injury.

    • Benedetta Bussolati
    •  & Giovanni Camussi
  • News and Views |

    Effectiveness of EGFR treatment is impaired through an early adaptive response. TNF–JNK–Axl–ERK signaling contributes to this primary resistance to EGFR inhibition and might serve as novel target to improve EGFR inhibition.

    • Rolf Warta
    •  & Christel Herold-Mende
    Nature Neuroscience 20, 1035–1037