During cellular senescence, cells eject mitochondrial DNA, sparking an inflammatory response that contributes to ageing. This process could be key in developing anti-ageing interventions.
October 2023 – Nature
- Mitochondrial DNA release: As cells enter senescence, a state where they no longer divide, they expel fragments of mitochondrial DNA into the surrounding cellular environment. This process is a fundamental aspect of cellular ageing
- Inflammatory response activation: The expelled mitochondrial DNA acts as a signal that activates the body’s immune response, leading to chronic inflammation. This kind of inflammation is increasingly recognised as a central feature of the ageing process, affecting the health and function of tissues
- SASP influence on ageing: The inflammatory signals are part of a broader set of changes known as the senescence-associated secretory phenotype (SASP). SASP includes the release of pro-inflammatory cytokines, growth factors, and proteases, which can disrupt the structure and function of tissues, contributing to the physical decline associated with ageing
- Therapeutic potential: Understanding the role of mitochondrial DNA in driving the SASP opens up new therapeutic possibilities. By finding ways to prevent or reverse this process, it may be possible to alleviate the detrimental effects of ageing on the body, potentially extending healthspan and delaying the onset of age-related diseases
Read the article at: Victorelli, S., Salmonowicz, H., Chapman, J. et al. Apoptotic stress causes mtDNA release during senescence and drives the SASP. Nature 622, 627–636 (2023). https://doi.org/10.1038/s41586-023-06621-4