Senescence articles within Nature

Featured

  • Article
    | Open Access

    During senescence, minority mitochondrial outer membrane permeabilization leads to the release of mtDNA into the cytosol through BAX and BAK macropores, in turn activating the cGAS–STING pathway, a major regulator of the senescence-associated secretory phenotype.

    • Stella Victorelli
    • , Hanna Salmonowicz
    •  & João F. Passos

  • Article |

    Mice overexpressing Has2 from the naked mole-rat showed an increase in hyaluronan levels in several tissues, and a lower incidence of spontaneous and induced cancer, attenuated inflammation through several pathways, extended lifespan and improved healthspan.

    • Zhihui Zhang
    • , Xiao Tian
    •  & Vera Gorbunova

  • Article |

    Through iterative cycles of viral challenge and rechallenge over ten years, mouse T cells are demonstrated to have essentially infinite potential for population expansion and longevity without malignant transformation or loss of functional competence.

    • Andrew G. Soerens
    • , Marco Künzli
    •  & David Masopust

  • Article
    | Open Access

    A lifetime cartography of in vivo senescent cells shows that they are heterogeneous. Senescent cells create an aged-like inflamed niche that mirrors inflammation associated with ageing and arrests stem cell proliferation and tissue regeneration.

    • Victoria Moiseeva
    • , Andrés Cisneros
    •  & Pura Muñoz-Cánoves

  • Article |

    Virus-induced senescence is a central pathogenic feature in COVID-19, and senolytics, which promote apoptosis of senescent cells, can reduce disease severity in hamsters,mice, as well as humans infected with SARS-CoV-2.

    • Soyoung Lee
    • , Yong Yu
    •  & Clemens A. Schmitt

  • Review Article |

    This Review examines the evidence showing that DNA damage is associated with ageing phenotypes, suggesting that it may have a central role as the cause of ageing.

    • Björn Schumacher
    • , Joris Pothof
    •  & Jan H. J. Hoeijmakers

  • Article |

    Chimeric antigen receptor (CAR) T cells targeting uPAR, a cell-surface protein that is upregulated on senescent cells, eliminate senescent cells in vitro and in vivo and reduce liver fibrosis in mice.

    • Corina Amor
    • , Judith Feucht
    •  & Scott W. Lowe

  • Article |

    During cellular senescence in human and mouse cells, L1 transposons become transcriptionally derepressed and trigger a type-1 interferon response, which contributes to age-associated inflammation and age-related phenotypes.

    • Marco De Cecco
    • , Takahiro Ito
    •  & John M. Sedivy

  • Letter |

    Cellular senescence induced by chemotherapy leads to the acquisition of stemness in cancer cells, which results in enhanced tumour-promoting capacity after forced release or spontaneous escape from the senescent cell-cycle arrest.

    • Maja Milanovic
    • , Dorothy N. Y. Fan
    •  & Clemens A. Schmitt

  • Letter |

    Cytoplasmic chromatin activates the innate immunity cytosolic DNA-sensing cGAS–STING pathway, leading both to short-term inflammation to restrain activated oncogenes and to chronic inflammation that associates with tissue destruction and cancer.

    • Zhixun Dou
    • , Kanad Ghosh
    •  & Shelley L. Berger

  • Article |

    When senescent cells accumulate during adulthood they negatively influence lifespan and promote age-dependent changes in several organs; clearance of these cells delayed tumorigenesis in mice and attenuated age-related deterioration of several organs without overt side effects, suggesting that the therapeutic removal of senescent cells may be able to extend healthy lifespan.

    • Darren J. Baker
    • , Bennett G. Childs
    •  & Jan M. van Deursen

  • Article |

    The regenerative properties of muscle stem cells decline with age as the stem cells enter an irreversible state of senescence; a study of mouse muscle stem cells reveals that entry into senescence is an autophagy-dependent process and promoting autophagy in old satellite cells can reverse senescence and restore their regenerative properties in an injury model.

    • Laura García-Prat
    • , Marta Martínez-Vicente
    •  & Pura Muñoz-Cánoves

  • Letter |

    In response to cancer-associated stress, autophagy machinery mediates degradation of nuclear lamina components in mammals, suggesting that cells might degrade nuclear components to prevent tumorigenesis.

    • Zhixun Dou
    • , Caiyue Xu
    •  & Shelley L. Berger

  • Letter |

    Neutrophil ageing, which encourages inflammation and vaso-occlusion in a mouse model of sickle-cell disease, is shown to depend on the intestinal microbiota and activation of the TLR/Myd88 signalling pathways.

    • Dachuan Zhang
    • , Grace Chen
    •  & Paul S. Frenette

  • Review Article |

    Cellular senescence has recently been shown to have roles in complex biological processes other than protection against cancer, and to represent a series of progressive and diverse cellular states after initial growth arrest; better understanding of mechanisms underlying its progression and of acute and chronic senescent cells may lead to new therapeutic strategies for age-related pathologies.

    • Jan M. van Deursen

  • Article |

    This study shows that ageing satellite cells undergo an irreversible transition from a quiescent to a pre-senescent state that results in the loss of muscle regeneration in sarcopenia; furthermore, increased expression of p16INK4a is identified as a common feature of senescent satellite cells.

    • Pedro Sousa-Victor
    • , Susana Gutarra
    •  & Pura Muñoz-Cánoves

  • Letter |

    Pyruvate dehydrogenase (PDH) is identified as a crucial mediator of BRAFV600E-induced cellular senescence: PDH is activated by BRAF-mediated suppression of PDK1, enhancing oxidative glucose metabolism, and PDK1 depletion eradicates mutant BRAF melanomas, indicating that this relationship between cell senescence and metabolism might be exploited therapeutically.

    • Joanna Kaplon
    • , Liang Zheng
    •  & Daniel S. Peeper

  • Outlook |

    Treating cognitive problems common in elderly people requires a deeper understanding of how a healthy brain ages.

    • Alison Abbott

  • Outlook |

    Researchers are learning about the molecular basis of ageing — and finding clues about how to treat diseases in the process.

    • Katherine Bourzac

  • Outlook |

    Why do some people cope better than others with getting old? Sociologist Eva Kahana, director of the Elderly Care Research Center at Case Western Reserve University, offers some clues.

    • Rebecca Kessler

  • Outlook |

    Scientists are searching for a genetic blueprint that will enable humans to stay healthy and vital well into their old age.

    • Michael Eisenstein

  • News & Views |

    Damaged cells can initiate cancer. To avert this, faulty cells disable their own propagation by undergoing senescence. But for full protection against liver cancer, the senescent cells must be cleared by the immune system. See Letter p.547

    • Manuel Serrano

  • News & Views |

    Age brings not just wisdom, but also, alas, many traits that to most of us are much less attractive. It now seems that, at least in mice, clearance of senescent cells delays some of the maladies associated with ageing. See Letter p.232

    • Daniel S. Peeper

  • Letter |

    Calcineurin inhibitors are the mainstay of immunosuppressive treatment for organ transplant recipients. However, treatment with these drugs commonly leads to squamous cell carcinoma (SCC) of the skin. It is shown here that an intact calcineurin/NFAT signalling pathway is important for suppressing SCC development. Inhibition of this pathway leads to increased expression of the ATF3 protein, which has a key role in tumorigenesis.

    • Xunwei Wu
    • , Bach-Cuc Nguyen
    •  & G. Paolo Dotto

  • Article |

    Cellular senescence — an irreversible cell-cycle arrest — has been implicated in suppressing tumour formation or growth. A new cellular signalling pathway that drives senescence has now been identified. This pathway does not involve most known mediators of senescence, and instead signals via the proteins Atf4, p27 and p21. Inactivating the proto-oncogene Skp2 in the context of oncogenic signalling can induce senescence through this new pathway, indicating that drugs that target Skp2 might be useful in cancer treatment.

    • Hui-Kuan Lin
    • , Zhenbang Chen
    •  & Pier Paolo Pandolfi

  • News & Views |

    Cellular senescence is a physiological mechanism for thwarting the proliferation of tumour cells. Encouraging cancer-prone cells to senesce might therefore be a way to nip this disease in the bud.

    • Manuel Serrano

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