Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/ijms23031512
Keywords
miRNA-1 (miR-1); miRNA-21 (miR-21); cardiovascular disease; myocardial ischemia-reperfusion injury; myocardial infarction; coronary artery disease; cardioprotection; cardiomyocytes; fibroblasts; immune cells
Funding
- National Institutes of Health [R01HL159865, R01HL147586]
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This review discusses the role of miR-1 and miR-21 in regulating myocardial apoptosis in ischemia-reperfusion injury, with a focus on different cardiac cell types including cardiomyocytes, fibroblasts, and immune cells. The therapeutic potential of miR-1 and miR-21 in preclinical studies is also examined.
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.
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