Figure 1.
ROS production from dysfunctional mitochondria as the driving force of cellular ageing.
ROS accelerates the onset of replicative senescence by increasing the rate of telomere shortening [42], [43] as well as feeding into a continuous DNA damage response that sustains the accumulation of inflammatory mediators as part of the senescence-associated secretory phenotype (SASP), and mitochondrial dysfunction, defined as enhanced production of superoxide together with (frequently) increased mitochondrial mass and decreased mitochondrial membrane potential. This maintains an irreversible state of persistent damage in senescent cells [22], [44]. The subsequent dysregulation of physiological function contributes to age-related pathology and/or carcinogenesis [45], [46].
Table 1.
Descriptive statistics of biomarker measurements.
Table 2.
Superoxide levels, mitochondrial mass and mitochondrial membrane potential in relation to other potential markers of oxidative stress induced cellular senescence.
Table 3.
Superoxide levels, mitochondrial mass and mitochondrial membrane potential in relation to informative BoA.
Figure 2.
Association between PBMC superoxide levels, mitochondrial mass, mitochondrial membrane potential and survival.
(Cox regression analysis)
Table 4.
Association between superoxide levels, mitochondrial mass, mitochondrial membrane potential and age-related outcomes.