Targeting the SASP to combat ageing: Mitochondria as possible intracellular allies?

被引:62
作者
Birch, Jodie [1 ]
Passos, Joao F. [1 ]
机构
[1] Newcastle Univ, Inst Ageing, Inst Cell & Mol Biosci, Campus Ageing & Vital, Newcastle Upon Tyne, Tyne & Wear, England
基金
英国生物技术与生命科学研究理事会;
关键词
ageing; mitochondria; SASP; senescence; senolytics; DNA-DAMAGE-RESPONSE; KAPPA-B ACTIVATION; SENESCENT CELLS; CELLULAR SENESCENCE; TELOMERE DYSFUNCTION; CLEARANCE; DEHYDROGENASE; ACCUMULATION; METABOLISM; GLYCOLYSIS;
D O I
10.1002/bies.201600235
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
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页数:7
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