Work

MitoQ reduces senescence burden in doxorubicin-treated endothelial cells by reducing mitochondrial ROS and DNA damage

Year: 2025

Type: article

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.

Source: American Journal of Physiology-Heart and Circulatory Physiology

DOI: 10.1152/ajpheart.00568.2025

Authors: Hossein Abdeahad, Denisse G. Moreno, Samuel I. Bloom, Lucas Norman, Lisa A. Lesniewski, Anthony J. Donato

Institutions: University of Utah, Salk Institute for Biological Studies, Westminster University, University of Westminster, Geriatric Research Education and Clinical Center

Language: English

Topic: Chemotherapy-induced cardiotoxicity and mitigation

Subfield: Cardiology and Cardiovascular Medicine

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: hybrid

Funders: American Cancer Society, U.S. Department of Veterans Affairs, Nora Eccles Treadwell Foundation, National Institutes of Health, National Institute on Aging, National Heart, Lung, and Blood Institute, National Cancer Institute, Veterans Affairs Scholarship Program

Awards: G150763035, Investigating novel intra- and extra-cellular regulators of telomere-mediated proliferative boundaries, G1952563938, G2067428092, G2615437256, G3338008254, G5447085330, G5562177406, Improving healthspan through discovery of potent NAMPT activators from a DNA-encoded library, G9000051283, G9000153163, G9000257828, G9000261771, G9000341470, Integrative Mechanisms of Vascular Aging, Tissue senescence and age-associated metabolic dysfunction: the role of immune cell mediated inflammation

OpenAlex ID: W4414645218

FWCI: 7.559

Cites: 33

Cited by: 12

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