Despite an active research activity since more than 30 years, there is no specific treatment nowadays against myocardial ischemia-reperfusion (IR) injury. Reperfusion injury occurs in the case of revascularization of the culprit artery in acute myocardial infarction (AMI) or after heart transplantation by paradoxically exacerbating injury after the abrupt return of oxygen. IR injury is mainly characterized, beside inflammation response, by calcium overload and mitochondrial production of reactive oxygen species leading to cell death of both cardiomyocytes and non-cardiomyocytes in particular vascular cells. Development of strategies based on inhibition of IR-induced cell death appeared as main contributors for the reduction of IR injury to provide cardioprotection in myocardial infarction or transplantation. However, despite numerous putative drugs identified in animal models, not one drug of potential clinical utility has emerged. This suggests that other strategies of translation need to be developed and that the concept of a “magic bullet” for a “magic single target” is probably exceeded. What are the new options available: discovering new targets with new technologies? Evaluating new drugs or association of drugs prepared with new formulations? Treating in a different time window? Using more relevant animal models with diabetes co-morbidity?
In this Research Topic, we invite contributions that both enhance our understanding of the pathophysiology of myocardial IR injury and that present the new therapeutic strategies that will protect the myocardium and decrease the morbi-mortality in patients by learning from past failures.
Reviews and original manuscript contributions may give new clues for the development of car-dioprotective strategies that will succeed in clinical setting. Papers may focus on the description of IR-induced cell death mechanisms including newly described mechanisms. Also they will focus on the development of cardioprotective strategies targeting these cascades including me-chanical, pharmacological, gene and cellular therapies, considering also the therapeutic time window appropriate for clinical applications. Approaches based on combination of existing therapies or considering big data technology may be considered. Finally, studies taken into account co-morbidities such as diabetes will be welcomed. Reports may concern basic science, preclinical, translational and clinical studies from bench to bed side and vice versa to increase the chance to translate.
Potential topics include:
1) An update or novel knowledge on myocardial ischemia-reperfusion (IR) injury from basic research, pre-clinical, as well as clinical research including also big data relevant for the understanding of the disease. Involvement of the microcirculation.
2) Description of cell death mechanisms and their regulatory pathways involved in myocardial ischemia-reperfusion (IR) injury.
3) New pharmacological tools or combination of drugs with pleiotropic cardioprotective effects.
4) New therapeutic strategies: gene therapy, gene editing, cell therapy and their extracellular-derived vesicles targeting cell death in IR injury.
5) Pre-clinical or clinical studies evaluating mechanisms and therapeutic strategies targeting IR-induced cell death in diabetes models
6) Devices improving survival after cardiac transplantation.
Despite an active research activity since more than 30 years, there is no specific treatment nowadays against myocardial ischemia-reperfusion (IR) injury. Reperfusion injury occurs in the case of revascularization of the culprit artery in acute myocardial infarction (AMI) or after heart transplantation by paradoxically exacerbating injury after the abrupt return of oxygen. IR injury is mainly characterized, beside inflammation response, by calcium overload and mitochondrial production of reactive oxygen species leading to cell death of both cardiomyocytes and non-cardiomyocytes in particular vascular cells. Development of strategies based on inhibition of IR-induced cell death appeared as main contributors for the reduction of IR injury to provide cardioprotection in myocardial infarction or transplantation. However, despite numerous putative drugs identified in animal models, not one drug of potential clinical utility has emerged. This suggests that other strategies of translation need to be developed and that the concept of a “magic bullet” for a “magic single target” is probably exceeded. What are the new options available: discovering new targets with new technologies? Evaluating new drugs or association of drugs prepared with new formulations? Treating in a different time window? Using more relevant animal models with diabetes co-morbidity?
In this Research Topic, we invite contributions that both enhance our understanding of the pathophysiology of myocardial IR injury and that present the new therapeutic strategies that will protect the myocardium and decrease the morbi-mortality in patients by learning from past failures.
Reviews and original manuscript contributions may give new clues for the development of car-dioprotective strategies that will succeed in clinical setting. Papers may focus on the description of IR-induced cell death mechanisms including newly described mechanisms. Also they will focus on the development of cardioprotective strategies targeting these cascades including me-chanical, pharmacological, gene and cellular therapies, considering also the therapeutic time window appropriate for clinical applications. Approaches based on combination of existing therapies or considering big data technology may be considered. Finally, studies taken into account co-morbidities such as diabetes will be welcomed. Reports may concern basic science, preclinical, translational and clinical studies from bench to bed side and vice versa to increase the chance to translate.
Potential topics include:
1) An update or novel knowledge on myocardial ischemia-reperfusion (IR) injury from basic research, pre-clinical, as well as clinical research including also big data relevant for the understanding of the disease. Involvement of the microcirculation.
2) Description of cell death mechanisms and their regulatory pathways involved in myocardial ischemia-reperfusion (IR) injury.
3) New pharmacological tools or combination of drugs with pleiotropic cardioprotective effects.
4) New therapeutic strategies: gene therapy, gene editing, cell therapy and their extracellular-derived vesicles targeting cell death in IR injury.
5) Pre-clinical or clinical studies evaluating mechanisms and therapeutic strategies targeting IR-induced cell death in diabetes models
6) Devices improving survival after cardiac transplantation.
