Natural Killer Cells in Post-Infarction Angiogenesis: Mechanisms, Evidence, and Translational Prospects

Myocardial infarction (MI) is leading cause of cardiovascular morbidity and mortality in developed and developing countries. Deep insight into the cellular and molecular mechanisms governing cardiac infarction may foster the translation of emerging therapeutic approaches into clinical practice. The promotion of angiogenesis and blood perfusion into the ischemic myocardium is essential for restoring functional cardiomyocytes after infarction. It has been indicated that different immune cell subsets can regulate the angiogenic switch in ischemic myocardium via close interaction with vascular cells and production of various pro-angiogenesis cytokines. Natural killer cells are innate lymphocytes that may influence inflammatory and reparative responses after MI. Depending on their phenotype and the stage of injury, NK cells may aggravate tissue damage or contribute to repair. These cells have capacity to be recruited into the inured sites with the capacity to mediate several molecular and cellular mechanisms associated with healing process by collaborating with other immune cells, production of various cytokines. However, the precise role of NK cells in regulating angiogenesis following myocardial infarction remains incompletely understood. In this regard, the elucidation of NK cell function and activity may pave the way for the development of long-term, efficient therapeutics with minimal side effects in MI patients. Here, we aimed to collect the recent data related to the activity of NK cells within the ischemic myocardium and the regulatory role of these cells in healing processes.