Mitochondrial dysfunction has been linked to both cellular senescence and ageing. Despite the relationship, it is still unclear whether mitochondria have a causal role in senescence. In this issue of The EMBO Journal, Correia‐Melo et al (2016) combine targeted depletion of mitochondria with impairment of their biogenesis to demonstrate that decreased numbers of mitochondria impair the senescence response. Their results suggest that targeting mitochondria could reduce the detrimental effects of senescence during ageing.
See also: C Correia‐Melo et al (April 2016)
Cellular senescence is a stress response in which damaged or ageing cells stop proliferating and undergo distinct changes in their transcription, chromatin organization and meta‐bolism. Senescent cells also produce a complex mix of secreted factors including matrix metalloproteinases, growth factors and pro‐inflammatory cytokines, collectively termed the senescence‐associated secretory phenotype (SASP) (Salama et al, 2014). The importance of mitochondria in cellular senescence has been linked to their ability to generate reactive oxygen species (ROS). ROS can affect cellular senescence by inducing or stabilizing the DNA damage response (DDR), leading to a permanent growth arrest. However, little is known about how mitochondrial ROS affect other features of senescence like the SASP. Moreover, the role of mitochondria in senescence extends beyond ROS production and other sources of ROS can also be …
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