MitoQ reduces senescence burden in doxorubicin-treated endothelial cells by reducing mitochondrial ROS and DNA damage
Hossein Abdeahad, Denisse G Moreno, Samuel I. Bloom, Lucas Norman, Lisa A. Lesniewski, Anthony J. Donato
Abstract
Doxorubicin (DOXO) is a widely used chemotherapy drug that can damage blood vessels and promote cardiovascular disease. This study shows that MitoQ, a mitochondria-targeted antioxidant, protects endothelial cells from DOXO-induced oxidative stress, DNA damage, and senescence. By preserving mitochondrial health, MitoQ may prevent vascular toxicity in cancer patients receiving DOXO, offering a potential strategy to improve cardiovascular outcomes in survivorship.
Topics & Concepts
DNA damageSenescenceMitochondrial ROSReactive oxygen speciesOxidative stressTelomereApoptosisUmbilical veinEndothelial dysfunctionDoxorubicinCell biologyBiologyPharmacologyEndothelial stem cellMitochondrionProgrammed cell deathSuperoxide dismutaseCancer researchChemistryReactive nitrogen speciesCell growthCellMitochondrial DNASuperoxideNeutrophil, Myeloperoxidase and Oxidative MechanismsElectron Spin Resonance StudiesNitric Oxide and Endothelin Effects