Cell death articles within Nature Cell Biology

Featured

  • News & Views |

    Diverse, specialized immune cells defend against pathogens and cancer cells. A new study reveals the comprehensive lipid compositions of these cells, with unique lipidomes associated with various immune cell types. They show that cell-specific lipid compositions determine a key functional phenotype: their susceptibility to ferroptosis.

    • Kandice R. Levental
    •  & Whitney S. Henry

  • News & Views |

    Progeria, or premature ageing, is a devastating condition caused by defects in the nuclear envelope and is associated with systemic inflammation. A study now shows in animal models that inhibiting necroptosis, and particularly activity of the RIPK1 kinase, reduces inflammation and results in a meaningful extension in lifespan1.

    • Panxue Wang
    •  & John Silke

  • Perspective |

    In this Perspective, Zhang discusses the latest advances in understanding of iron function, regulation and metabolism, as well as the implications for ferroptosis in health and disease.

    • Donna D. Zhang

  • Review Article |

    In this Review, Dai, Stockwell, Kroemer, Tang and colleagues offer a comprehensive discussion of the molecular regulation of ferroptosis and highlight how this may be potentially leveraged for therapeutic benefit for disease treatment.

    • Enyong Dai
    • , Xin Chen
    •  & Daolin Tang

  • Comment |

    Cell death is an important biological process whose experimental detection and measurement can be difficult, especially when examining many conditions in parallel. The interpretation of cell death data is complicated by the diversity of measurement techniques and lack of standardized methods in the field. Here, we offer tips to help interpret cell death experiments.

    • Scott J. Dixon
    •  & Michael J. Lee

  • News & Views |

    The main barriers for intracellular receptors to sense circulating pathogen-associated molecular patterns (PAMPs) is how these PAMPs enter the cells. A study reveals that extracellular vesicles (EVs) bind lipopolysaccharide (LPS) via the lipid bilayer and mediates LPS intracellular transfer in a CD14-dependent endocytosis to activate noncanonical NLRP3 inflammasome and pyroptosis.

    • Yi Huang
    •  & Rongbin Zhou

  • News & Views |

    The PHD–pVHL pathway is essential for oxygen-dependent prolyl hydroxylation of HIFA. A recent study identifies RIPK1 as a hydroxylation target in this pathway during hypoxia-induced cell death and presents a 2.8 Å resolution crystal structure of the pVHL–elongin B/C complex bound to hydroxylated RIPK1.

    • Wei Ruan
    • , Holger K. Eltzschig
    •  & Xiaoyi Yuan

  • News & Views |

    A new study shows that the enzymes involved in de novo pyrimidine synthesis and ferroptosis form a complex called the pyrimidinosome, which is controlled by AMPK. Cancer cells low in AMPK expression rely on the pyrimidinosome, suggesting that co-inhibition of AMPK and the pyrimidinosome represents a potential cancer treatment strategy.

    • Matthew Dodson
    •  & Donna D. Zhang

  • News & Views |

    The selenoprotein glutathione peroxidase 4 (GPX4) is the guardian of ferroptosis, a form of cell death earmarked by unrestrained lipid peroxidation. A new study shows that the metabolic enzyme creatinine kinase B (CKB) phosphorylates GPX4, which may influence the susceptibility of cancer cells to ferroptosis.

    • Eikan Mishima
    •  & Marcus Conrad

  • Article |

    Liu, Nie et al. identify disulfidptosis as a form of cell death resulting from aberrant accumulation of disulfide bonds in actin cytoskeleton proteins that is induced following glucose starvation and dependent on SLC7A11-mediated cystine uptake.

    • Xiaoguang Liu
    • , Litong Nie
    •  & Boyi Gan

  • News & Views |

    Extramitochondrial coenzyme Q (CoQ) can function as a potent anti-ferroptosis radical trapper. However, it is largely unknown how CoQ is transported from mitochondria to the plasma membrane. A study now suggests that PARL-mediated STARD7 processing is responsible for the cellular distribution of CoQ.

    • Deguang Liang
    •  & Xuejun Jiang

  • News & Views |

    NADPH levels serve as a biomarker of sensitivity to ferroptosis, but the regulators that detect cellular NADPH levels and modulate downstream ferroptosis responses are unknown. A study now identifies MARCHF6 in the ubiquitin system as an NADPH sensor that suppresses ferroptosis.

    • Chao Mao
    •  & Boyi Gan

  • News & Views |

    Necrosomes formed by RIPK1–RIPK3 mediate necroptosis. Super-resolution microscopy identifies the architectural features of necrosomes and provides mechanistic insights into the signalling from RIPK1 to RIPK3 when RIPK1 is activated to mediate necroptosis, and from RIPK3 to RIPK1 when RIPK3 is inhibited to mediate apoptosis.

    • Weiwei Qi
    •  & Junying Yuan

  • News & Views |

    Lipid metabolism is crucial for the execution of ferroptosis. A new study demonstrates that the function of the lipid metabolic enzyme ACSL4 is positively regulated by phosphorylation, leading to amplification of ferroptotic cell death. These results shed new light on the regulation of ferroptosis execution in cancer cells.

    • Jason Rodencal
    •  & Scott J. Dixon

  • Article |

    Through CRISPR–Cas9 and kinase inhibitor screening, Zhang et al. show that PKCβII phosphorylates and activates ACSL4 to enhance polyunsaturated fatty acid-containing lipid biosynthesis, thereby promoting accumulation of lipid peroxidation and ferroptosis.

    • Hai-Liang Zhang
    • , Bing-Xin Hu
    •  & Xiao-Feng Zhu

  • News & Views |

    A form of programmed cell death, necroptosis, in intestinal epithelial cells initiates mucosal inflammation. A study now finds that prostanoid EP4 receptor signalling interferes with RIPK1–RIPK3-dependent MLKL activation, thereby inhibiting necroptosis and accelerating resolution of inflammation.

    • Nicole C. Kaneider
    •  & Arthur Kaser

  • Article |

    Baumgartner et al. identify proteotoxic stress as the underlying cause of the loser status in a cell competition model caused by reduced autophagic, proteasomal flux and accumulation of protein aggregates.

    • Michael E. Baumgartner
    • , Michael P. Dinan
    •  & Eugenia Piddini

  • News & Views |

    Programmed death ligand-1 (PD-L1) is well known for its role as an immune checkpoint regulator, but little is known about its function in other cellular processes. A study now shows that in tumour cells PD-L1 mediates pyroptosis, an inflammatory form of cell death, by activating the expression of Gasdermine C, ultimately leading to tumour necrosis.

    • María Teresa Blasco
    •  & Roger R. Gomis

  • News & Views |

    Ferroptosis is an iron-dependent mode of cell death driven by lipid peroxidation, capable of explosively propagating through a field of cells. Two studies now explore the mechanisms underlying ferroptotic cell death and its spread, as well as its possible in vivo significance, shedding light on some of the burning questions surrounding ferroptosis.

    • Andrew J. Davidson
    •  & Will Wood

  • Article |

    Lee et al. show that energy stress inhibits ferroptosis through AMPK activation and demonstrate a role for AMPK in ferroptosis-associated renal ischaemia–reperfusion injury in vivo.

    • Hyemin Lee
    • , Fereshteh Zandkarimi
    •  & Boyi Gan

  • News & Views |

    Loss-of-function mutations in the ubiquitin ligase Parkin are a cause of Parkinson’s disease. Parkin also has tumour-suppressor activity, although how Parkin prevents cancer is unclear. Unexpectedly, Parkin is found to suppress cancer by inhibiting an inflammatory type of cell death called necroptosis.

    • Kai Cao
    •  & Stephen W. G. Tait

  • News & Views |

    Healthy and malignant haematopoietic stem cells (HSCs) must overcome a variety of cell intrinsic and extrinsic stresses to maintain their functionality. Now, IRE1α –XBP1 signalling is shown to protect HSCs and to promote survival of, and confer competitive advantages to, NRAS-mutated pre-leukaemic cells.

    • Marina Scheller-Wendorff
    •  & Carsten Müller-Tidow

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