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Figure 2 | Longevity & Healthspan

Figure 2

From: Telomeres, oxidative stress and inflammatory factors: partners in cellular senescence?

Figure 2

Two different models by which reactive oxygen species can impact on cellular senescence. (a) Reactive oxygen species (ROS) produced via mitochondrial and non-mitochondrial sources can induce genomic DNA damage and accelerate telomere erosion/damage, both of which contribute to activation of a DNA damage response (DDR). (b) ROS can act as signalling molecules in senescence: activation of “senescence signals” has been shown to result in increased ROS generation (mitochondrial and non-mitochondrial). ROS has been shown to impact on a variety of pathways which may help stabilise the senescence growth arrest. (c) Simplified feedback loop model involving ROS and DNA damage. Telomere uncapping or general DNA damage triggers a DDR which culminates through yet unidentified processes to ROS generation. ROS generation leads to additional DNA damage to the genome, stabilising the DDR and leading to a stable senescence arrest.

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