title: Targeting the SASP to combat ageing: Mitochondria as possible intracellular allies?
abstract: Anti-senescence therapies, such as drugs that specifically kill senescent cells, to stave off ageing are currently under investigation. While these interventions show promise, their potential pitfalls are discussed herein. We have shown that the mitochondria are essential for development of senescence and many of the associated phenotypes, including the often detrimental senescence-associated secretory phenotype (SASP). Here, we disentangle many ways in which the mitochondria may influence senescence and development of the SASP and focus on possible pathways that could be exploited for future generation of anti-senescence therapies with a clear aim; to specifically eliminate the problematic features of senescent cells, while maintaining their beneficial characteristics.
authors.affiliation: Institute for Cell and Molecular Biosciences, Campus for Ageing and Vitality, Newcastle University Institute for Ageing, Newcastle University, Newcastle Upon Tyne, UK.
authors.forename: Jodie
authors.initials: J
authors.lastname: Birch
authors.affiliation: Institute for Cell and Molecular Biosciences, Campus for Ageing and Vitality, Newcastle University Institute for Ageing, Newcastle University, Newcastle Upon Tyne, UK.
authors.forename: João F
authors.initials: JF
authors.lastname: Passos
mesh_terms: D000375:Aging / Q000235:genetics / Q000378:metabolism*; D000067531:Alarmins / Q000378:metabolism; D000818:Animals; D016922:Cellular Senescence / Q000235:genetics / Q000502:physiology; D004249:DNA Damage; D006801:Humans; D008928:Mitochondria / Q000235:genetics / Q000378:metabolism*; D008954:Models, Biological; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: D000067531:Alarmins; D058570:TOR Serine-Threonine Kinases
keywords: SASP; ageing; mitochondria; senescence; senolytics