Ischemia-reperfusion (I/R) injury, the paradoxical tissue response that is manifested by blood flow-deprived and oxygen-starved organs following the restoration of blood flow and tissue oxygenation, is one of the major causes of high morbidity, disability, and mortality. During I/R injury, mitochondrial dysfunction and excessive reactive oxygen species (ROS) produced by cells or lesions contribute to tissue injury. Mitochondrial dysfunction and oxidative stress are also involved in a variety of vascular diseases, such as atherosclerosis and aortic dissection/aneurysm. As an important process of pathogenesis, oxidative stress promotes both I/R injury and the development of vascular diseases through organic damage or failure and cellular injury or death. Mitochondria, as primary energy suppliers, are associated with pathologic changes in many disorders. Antagonists targeting oxidative stress and mitochondrial disturbances have been developed and used to evaluate curative effects for human diseases including I/R injury and vascular diseases in a series of in vivo studies and human trials. Given that oxidative stress and mitochondrial disturbances are closely related to I/R injury and vascular diseases, it is vital to gain further insight into their roles in such disorders.

Oxidative stress and mitochondrial disturbances play a critical role in I/R injury and vascular diseases, which provide opportunities for prevention and treatment in such disorders. However, there are many outstanding questions about I/R injury and vascular diseases. The detailed mechanism of the role of oxidative stress and mitochondrial disturbances in I/R injury and vascular diseases is yet to be revealed and needs further in-depth investigation. To date, the therapeutic or prophylactic strategies targeting oxidative stress and mitochondrial disturbances are still lacking. More in vivo studies and human trials focused on oxidative stress and mitochondrial disturbances are needed. Furthermore, regulatory factors in the upstream and downstream signaling pathways related to oxidative stress and mitochondrial disturbances remain to be explored.

In this Special Issue, we invite investigators to contribute original research as well as review articles to discuss the pathological effects and the underlying mechanisms of oxidative stress and mitochondrial disturbances in I/R injury and vascular diseases. Searching for specific and effective molecules and targets will be helpful for improving the clinical treatment of I/R injury and vascular diseases. Therefore, we encourage authors to submit integrative and novel insights to improve current treatments and precautions.

Potential topics include but are not limited to the following:

• I/R injury not limited to myocardial ischemia reperfusion, but also in other organs such as the kidney and liver
• Recent advances in the role of oxidative stress and mitochondria in I/R injury or vascular diseases
• The important progress in I/R injury or vascular diseases
• Clinically relevant data and basic research about diagnostic markers, therapeutic effects, and prognostic indicators of I/R injury or vascular diseases with a focus on oxidative stress or mitochondria
• Ferroptosis in I/R injury or vascular diseases
• Human studies of I/R injury and vascular diseases involving oxidative stress and mitochondrial dysfunction
• Innovative insights into underlying mechanisms of I/R injury and vascular diseases in the field of oxidative stress and mitochondria