Oxidized phosphatidylcholines trigger ferroptosis in cardiomyocytes during ischemia-reperfusion injury

Author:

Stamenkovic Aleksandra1,O’Hara Kimberley A.1,Nelson David C.1,Maddaford Thane G.1,Edel Andrea L.1,Maddaford Graham1,Dibrov Elena1,Aghanoori MohamadReza23,Kirshenbaum Lorrie A.1,Fernyhough Paul23,Aliani Michel45ORCID,Pierce Grant N.15,Ravandi Amir16

Affiliation:

1. Institute of Cardiovascular Sciences, Department of Physiology and Pathophysiology, St. Boniface Hospital, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada

2. Department of Pharmacology and Therapeutics, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada

3. Division of Neurodegenerative Disorders, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, Canada

4. Department of Food and Human Nutritional Sciences, University of Manitoba, Winnipeg, Canada

5. The Canadian Centre for Agri-Food Research in Health and Medicine, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, Canada

6. Department of Internal Medicine, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada

Abstract

Oxidized phosphatidylcholines (OxPC) generated during reperfusion injury are potent inducers of cardiomyocyte death. Our studies have shown that OxPCs exert this effect through a ferroptotic process that can be attenuated. A better understanding of the OxPC cell death pathway can prove a novel strategy for prevention of cell death during myocardial reperfusion injury.

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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