This Research Topic is the second volume of the topic, “New Strategies to Inhibit Cell Death in Myocardial Ischemia-Reperfusion Injury; How to succeed?”. Please see the first volume
here.
Despite active research activity for more than 30 years, there is currently no specific treatment against myocardial ischemia-reperfusion (IR) injury. Restoration of blood flow is the only treatment recommended for the salvage of ischemic tissues. However, abrupt return of oxygen in the ischemic area triggers IR injury, and is mainly characterized by the inflammatory burst, calcium overload, and mitochondrial production of reactive oxygen species, leading to cell death of both cardiomyocytes and non-cardiomyocytes (such as vascular cells). Strategies to target specifically cell death need to be developed to prevent reperfusion injury during myocardial infarction or organ transplantation. To date, despite numerous putative drugs identified in animal models, not one drug of potential clinical utility has emerged. This suggests that other strategies for the clinical 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 cell death mechanisms involved in myocardial IR injury, and that present new therapeutic strategies to protect the myocardium and decrease morbi-mortality rates in patients by learning from past failures. We welcome the submission of review and original research articles that may give new insights into the development of cardioprotective strategies that will succeed in the clinical setting. Papers submitted to the collection may focus on the description of IR-induced cell death mechanisms involved in myocardial damage associated with Coronavirus disease 2019 (COVID-19). Articles will focus on the development of cardioprotective strategies targeting these cascades including mechanical, 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, articles presenting results on large animals are highly encouraged and studies taken into account aging or co-morbidities such as diabetes and obesity will be welcome. Research may concern basic science, preclinical, translational, and clinical studies from bench to bed side and vice versa to increase the chance to translate in the clinical practice.
Potential subtopics of research may include:
1) An update or novel knowledge on myocardial ischemia-reperfusion (IR) injury from basic research, pre-clinical, as well as clinical research including vascular complications.
2) Description of cell death mechanisms and their regulatory pathways involved in myocardial ischemia-reperfusion (IR) injury in cardiomyocytes and non-cardiomyocytes. Influence of aging, diabetes or COVID-19.
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) Preclinical or clinical studies evaluating mechanisms and therapeutic strategies targeting IR-induced cell death in animal models including large species and considering co-morbidities such as aging and diabetes
6) Devices improving survival after cardiac transplantation.
