Abstract
Introduction: Globally, Myocardial Ischemia or Ischemic Heart Disease (IHD) inflicts 126 million individuals, totaling an estimated nine million deaths annually. IHD injury and healing are characterized by recruitment of several immune cell types to the cardiac tissue. In addition, atherosclerosis, a common causative factor of IHD, is initiated by mediators of innate and adaptive immunity, thus providing the rationale for studying the role of immune cell types in myocardial ischemia. Clarifying the functions and interactions among these cell types will inform drug targeting studies and ultimately facilitate development of IHD treatment and prevention approaches. Methods: This systematic review highlights and summarizes pertinent studies evidencing the function and interaction of macrophages, monocytes, lymphocytes, platelets, and endothelial cells in IHD pathology. Electronic databases searched consist of Ovid, PubMed, Google Scholar, Web of Science, and ScienceDirect. Keywords include: “immune cells”, “innate immunity”, “inflammation”, “cardiac macrophages”, “adaptive immunity”, “lymphocytes”, “B cells”, “T cells”, “T-regulatory cells”, “myocardial infarction”, “reperfusion”, and additional related keywords. Results: Macrophages, monocytes, lymphocytes, platelets, and endothelial cells interact under innate and adaptive immune responses to initiate and sustain inflammation in cardiac tissue. Sustained inflammation signals for the recruitment of associated molecules to the site of ischemic heart damage which instigate injury and healing processes. Discussion: Building a comprehensive picture of interacting cell types enables the identification of druggable targets and potential treatment and prevention options. Here, we propose several steps of IHD pathology during which further studies with agonist and inhibitor molecules may yield fruitful treatment directions. Lastly, we discuss study limitations and future research avenues. Conclusions: Overall, explicating the immune cell type function and interactions will build a connective understanding of IHD pathology. In turn, elucidating the molecular and cell-specific mechanisms of the inflammatory immune response in cardiomyopathies will aid in the modelling of IHD disease progression as well as facilitate the identification of potential biomarkers and druggable targets to alleviate heart failure disease burden.
Highlights
Myocardial Ischemia or Ischemic Heart Disease (IHD) inflicts 126 million individuals, totaling an estimated nine million deaths annually
We discuss data indicating the role of macrophages, monocytes, lymphocytes, platelets, and endothelial cells in the inflammatory process to explicate a basis upon which future therapeutic options may see renewed interest
Preliminary evidence using flow cytometry-based immunophenotyping indicate the presence of macrophages in myocytes, suggesting that in a steady-state heart, cardiac macrophages are in direct contact with endothelial cells and myocytes [20]
Summary
Myocardial Ischemia or Ischemic Heart Disease (IHD) inflicts 126 million individuals, totaling an estimated nine million deaths annually. IHD injury and healing are characterized by recruitment of several immune cell types to the cardiac tissue. Atherosclerosis, a common causative factor of IHD, is initiated by mediators of innate and adaptive immunity, providing the rationale for studying the role of immune cell types in myocardial ischemia. Clarifying the functions and interactions among these cell types will inform drug targeting studies and facilitate development of IHD treatment and prevention approaches. Referred to as coronary artery disease (CAD), IHD often clinically manifests as ischemic cardiomyopathy (CM) and myocardial infarction (MI), or damaged cardiac muscle cells and heart attack, respectively [1,2].
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