Mitochondrial elongation is observed on entering senescence in many cell types — but the functional consequence of this change in mitochondrial dynamics has been unclear. Marina Jendrach and colleagues now report that mitochondrial elongation in senescent cells enables resistance to oxidative stress (p. 917): senescent cells are resistant to mitochondria-targeted photodamage, whereas young cells exhibit mitochondrial fragmentation and a loss of mitochondrial membrane potential upon the same treatment. Notably, mitochondrial elongation in senescent cells correlates with decreased expression of two mitochondrial fission factors, Drp1 and Fis1. Furthermore, compared with young cells, senescent cells express higher levels of a ubiquitous kinase known as PINK1; mutations in PINK1 have been linked to neuropathology in Parkinson's disease (PD). PINK1 does not seem to be directly involved in mitochondrial fission or fusion events, but knockdown of its expression makes senescent cells prone to photodamage. Finally, the authors show that decreased expression of Drp1 and Fis1 is required for increased PINK1 expression in senescent cells. Therefore, alterations in mitochondrial dynamics via Drp1 and Fis1 trigger a PINK1-mediated protective mechanism in senescent cells that, when dysregulated, might contribute to the progression of age-related diseases, including PD.