Joel Riley

Jan 2, 2024 | nature.com | Stella G. Victorelli |James Chapman |Joel Riley |Diana Jurk |Lilian Sales Gomez |Joshua N Farr | +11 more

Correction to: Nature https://doi.org/10.1038/s41586-023-06621-4 Published online 11 October 2023In the version of this article initially published, US NIH grants R33AG61456-4 and R01AG064165 were missing from the Acknowledgements section and have now been inserted in the HTML and PDF versions of the article.

Oct 11, 2023 | nature.com | Stella G. Victorelli |James Chapman |Joel Riley |Diana Jurk |Lilian Sales Gomez |Joshua N Farr | +11 more

AbstractSenescent cells drive age-related tissue dysfunction partially through the induction of a chronic senescence-associated secretory phenotype (SASP)1. Mitochondria are major regulators of the SASP; however, the underlying mechanisms have not been elucidated2. Mitochondria are often essential for apoptosis, a cell fate distinct from cellular senescence. During apoptosis, widespread mitochondrial outer membrane permeabilization (MOMP) commits a cell to die3.