Journal
CHEMICO-BIOLOGICAL INTERACTIONS
Volume 303, Issue -, Pages 35-39Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.cbi.2019.01.032
Keywords
Doxorubicin cardiotoxicity; Oxidized phospholipids; Oxidized phosphatidylcholines; Cardiolipin; Inflammation; Ferroptosis
Funding
- Canadian Institutes of Health Research [FRN-74733]
- Heart and Stroke Foundation [G-14-0006050]
- Research Manitoba 983
- Bank of Montreal studentship award
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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.
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