About this Research Topic
Reperfusion injury induces several responses at the cardiovascular, pulmonary, cerebrovascular and metabolic levels, which may lead to chronic diseases and increased morbidity and mortality. The initial responses to hypoxia are a compensatory response that induces activation of protective mechanisms. However, when hypoxia is prolonged, the chronic activation of cellular responses induces long-lasting modifications that may result in maladaptive changes with increased cardio, cerebrovascular and metabolic risk.
In this view, acute and chronic hypoxic conditions have an increased risk and prevalence of cardiovascular, neurological and liver dysfunction, such as pulmonary hypertension, heart failure, hypoxic, perinatal asphyxia, stroke and liver ischemia-reperfusion. Similar responses are seen in clinical patients exposed to acute and chronic hypoxia, but the intensity of the physiological response would determine the cellular mechanisms that are activated. However, short-term and long-lasting effects are still unclear.
Pharmacological strategies have been proven to be reproducible in preclinical studies across a range of studies with in vitro and ex vivo experimental models. Still, new pharmacological strategies should be further tested in in vivo and controlled clinical settings (for example, cardiac and liver ischemia-reperfusion injury). Further, once a proposed drug is tested in clinical trials, the possible interferences with the hypoxic exposure need to be evaluated to confirm whether the intervention is truly effective in some clinical patients. Animal experiments, observational studies and randomized clinical trials that have examined the protective effects of pharmacological preconditioning and clinical evidence that support an associated molecular mechanism are not currently well characterized.
This Research Topic welcomes Original Research and Review articles that focus on animal models and clinical interventions about the pathophysiology of reperfusion injury, in acute and chronic hypoxic conditions. In addition, reference will be made to current preconditioning strategies and their efficacy against structural and functional consequences.
In particular, this article collection is focused on the following topics:
- Cardiac reperfusion injury in animals and clinical settings such as ischemic cardiomyopathy and reperfusion arrhythmias.
- Current concepts of pathophysiology and therapies in cardiac ischemic and pharmacological preconditioning.
- Mechanisms about liver preconditioning in animal and clinical model of ischemia-reperfusion injury.
- Kidney ischemia-reperfusion injury in animal and clinical model, molecular targets and pharmacological modulation.
- Current concepts of pathophysiology and therapies in cerebral ischemia and reperfusion injury.
- Molecular mechanisms associated with the pathophysiology of graft versus host disease and their pharmacological modulation.
- Mechanisms and prevention of lung ischemia-reperfusion injury in lung transplantation.
- Ex vivo models to reduce ischemia-reperfusion injury in organs for transplantation.
- Role of ischemia-reperfusion injury in sepsis: mechanisms and potential therapeutic target.
- Role of microRNAs in the regulation of ischemia-reperfusion injury: mechanisms and possible therapeutic targets.
- Clinical preconditioning strategies in cardiopulmonary rehabilitation.
Keywords: Reperfusion Injury, Animal Model, Clinical Model, Metabolic Risk, Pharmacological Strategies
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