Senescent cells: an emerging target for diseases of ageing

By Bennett G. Childs, Martina Gluscevic, D. Baker, Rémi-Martin Laberge, D. Marquess, J. Dananberg, Jan M. van Deursen. Nature reviews. Drug discovery, 2017

1,101 citations recorded by the source corpus.

Chronological age represents the single greatest risk factor for human disease. One plausible explanation for this correlation is that mechanisms that drive ageing might also promote age-related diseases. Cellular senescence, which is a permanent state of cell cycle arrest induced by cellular stress, has recently emerged as a fundamental ageing mechanism that also contributes to diseases of late life, including cancer, atherosclerosis and osteoarthritis. Therapeutic strategies that safely interfere with the detrimental effects of cellular senescence, such as the selective elimination of senescent cells (SNCs) or the disruption of the SNC secretome, are gaining significant attention, with several programmes now nearing human clinical studies.

Subfields: Dermatology, Immunology, Physiology

View Paper: https://www.semanticscholar.org/paper/7c1710ccf393241b4c14c2632da932c5f15d8804

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Citations in the corpus

Measuring biological aging in humans: A quest (2019, background): “…shortening, metabolic and proteostatic stress, reactive oxidative species (ROS), oncogene activation, mitochondrial dysfunction, epigenetic changes, and other mechanisms that have not been fully clarified (Childs, Durik, Baker, & van Deursen, 2015; Childs et al., 2017; López-Otín et al., 2013).”
Mitochondrial metabolism and cancer (2017, background): “Besides triggering RCD, oncogene activation can also promote a permanent proliferative arrest known as cellular senescence, generally as a result of increased oxidative stress [58].”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “however, casts doubts on the actual feasibility of this approach [958, 968].”
Kidney fibrosis: from mechanisms to therapeutic medicines (2023, background): “Cellular senescence is a fate where cell cycle arrest is permanent and irreversible.(86) The p16 and p53-p21 are both critical cyclin-dependent kinase (CDK) inhibitors, leading to cellular senescence.”
Aging and aging-related diseases: from molecular mechanisms to interventions and treatments (2022, background): “However, the levels of CDK4 in NAFLD patients are increased in an age-dependent manner.(316) In addition, senescent hepatocytes exhibit specific metabolic dysregulation and mitochondrial dysfunction, which have been linked to NAFL pathogenesis.”