Cyclosporine A normalizes mitochondrial coupling, reactive oxygen species production, and inflammation and partially restores skeletal muscle maximal oxidative capacity in experimental aortic cross-clamping

Aortic cross-clamping increases reactive oxygen species production and impairs skeletal muscle mitochondrial function. Even subtle muscle impairments may increase morbidity after abdominal aortic aneurysm repair, supporting a need for muscle protection during vascular surgery. Albeit its protective effects might be related to muscle content in cyclophilin D, this study demonstrates that cyclosporine A significantly alleviates ischemia-reperfusion injury in skeletal muscle. Because cyclosporine A can be used safely in humans, it might be an alternative or a synergistic therapeutic approach to ischemic preconditioning in order to reduce mitochondrial dysfunction and reactive oxygen species production in vascular patients undergoing aortic cross-clamping.