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• W2911295209 abstract "Doxorubicin (Dox), a widely used chemotherapy drug, can also cause cardiotoxic effects leading to heart failure. The excessive oxidative stress caused by Dox results in the modification of a variety of cellular molecules, including phospholipids. In cardiomyocytes, Dox increases oxidation of a species of phospholipids, phosphatidylcholine, which has been associated with increased cell death. Oxidized phospholipids (Ox-PL) are involved in development and progression of various pathologies, including atherosclerosis, thrombosis, and tissue inflammation. Moreover, Ox-PL and excess iron are associated with ferroptosis, a form of regulated cell death. Neutralizing Ox-PL increases resistance to ischemia-reperfusion injuries which is linked to preservation of the mitochondrial membrane potential. This review aims to discuss the potential role of Ox-PL in Dox-induced pathology and supports the notion that a better understanding of the field could point to new strategies to prevent cardiotoxicity." @default.
• W2911295209 created "2019-02-21" @default.
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• W2911295209 date "2019-04-01" @default.
• W2911295209 modified "2023-10-12" @default.
• W2911295209 title "Oxidized phospholipids in Doxorubicin-induced cardiotoxicity" @default.
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• W2911295209 doi "https://doi.org/10.1016/j.cbi.2019.01.032" @default.
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