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.