Loss of cyclophilin D prolyl isomerase activity desensitizes mitochondrial permeability transition pore opening in isolated cardiac mitochondria, but does not protect in myocardial ischemia-reperfusion injury

J Mol Cell Cardiol. 2023 Oct:183:67-69. doi: 10.1016/j.yjmcc.2023.09.003. Epub 2023 Sep 9.

¹ Laboratory of Cardiac Physiology, Cardiovascular Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA. Electronic address: CasinKM@nih.gov.
² Laboratory of Cardiac Physiology, Cardiovascular Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA.
³ Transgenic Core, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD, 20892, USA.
⁴ Deptartment of Medicine, Albert Einstein College of Medicine and Cell Biology and Wilf Family Cardiovascular Research Institute, Bronx, NY 10461, USA.

No abstract available

Keywords: Cyclophilin D; Cyclosporine A; Ischemia-reperfusion injury; Mitochondria permeability transition pore; Prolyl isomerase.

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