Dear Colleagues,

Ischemia and reperfusion–elicited tissue injury contributes to morbidity and mortality in a wide range of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest, sickle cell disease and sleep apnea. Ischemia-reperfusion injury is also a major challenge during organ transplantation and cardiothoracic, vascular and general surgery. An imbalance in metabolic supply and demand within the ischemic organ results in profound tissue hypoxia and microvascular dysfunction. Subsequent reperfusion further enhances the activation of innate and adaptive immune responses and cell death programs. The generation of reactive oxygen species (ROS) increases due to a lower concentration of antioxidative agents in ischemic cells. ROS cause oxidative stress that promotes endothelial dysfunction, DNA damage, and local inflammatory responses. Inflammatory cascades and oxidative stress may subsequently induce a cytokine storm, resulting in cell death caused by damage to cellular structures. The reperfusion stage is dynamic and may persist for several days. Understanding the detailed mechanism of ischemia-reperfusion injury may provide a strong foundation not only for novel therapeutic opportunities, but also for injury prevention.

The current Special Issue focuses on molecular and cellular mechanisms underlining pathogenesis and novel therapeutic approaches targeting the ischemia and reperfusion injuries. We welcome research or review articles focusing on the topics.

Prof. Dr. Rosanna Di Paola
Dr. Enrico Gugliandolo
Dr. Roberta Fusco
Guest Editors

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• molecular mechanism
• biochemistry
• One Health
• animals
• toxicology