Abstract
Coronary artery disease remains the leading cause of death. Acute myocardial infarction (MI) is characterized by decreased blood flow to the coronary arteries, resulting in cardiomyocytes death. The most effective strategy for treating an MI is early and rapid myocardial reperfusion, but restoring blood flow to the ischemic myocardium can induce further damage, known as ischemia-reperfusion (IR) injury. Novel therapeutic strategies are critical to limit myocardial IR injury and improve patient outcomes following reperfusion intervention. miRNAs are small non-coding RNA molecules that have been implicated in attenuating IR injury pathology in pre-clinical rodent models. In this review, we discuss the role of miR-1 and miR-21 in regulating myocardial apoptosis in ischemia-reperfusion injury in the whole heart as well as in different cardiac cell types with special emphasis on cardiomyocytes, fibroblasts, and immune cells. We also examine therapeutic potential of miR-1 and miR-21 in preclinical studies. More research is necessary to understand the cell-specific molecular principles of miRNAs in cardioprotection and application to acute myocardial IR injury.
Highlights
Coronary artery disease remains the leading cause of death for both men and women of most ethnicities in the United States [1,2]
Key findings from this study revealed that a single miRNA, hsa-miR-21, causally links ischemia reperfusion injury in the heart to coronary artery disease, stroke and obesity [13]
Cnx43 in H9C2 cells subjected to HR injury; Telmisartan ↑ B-cell lymphoma 2 (Bcl-2) and
Summary
Coronary artery disease remains the leading cause of death for both men and women of most ethnicities in the United States [1,2]. The purpose of the miRNA clusters is to potentially regulate every aspect of cellular function, including growth, development, cell death, among others [9] Overall, these miRNAs have a profound impact on cardiac pathology and, when dysregulated, contribute to the disease, as is the case in acute myocardial IR injury [10,11,12]. The study by Pan et al established that miR-1 plays an important role in cardiac injury, and reducing miR-1expression effectively mitigates the myocardial injury These studies demonstrate mixed conclusions about the effects of miR-1 on IR injury (Table 1), most likely explained by differences due to reperfusion times or disease models.
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