Key result
MicroRNAs regulate myocardial infarction through apoptosis, autophagy, proliferation, and inflammation, offering potential applications in stem cell therapy and clinical diagnosis.
Why the study?
Patients experiencing ischemic infarction often suffer irreversible cardiac damage despite vascular reflow, prompting investigation into the regulatory mechanisms and therapeutic potential of microRNAs.
MicroRNAs play a critical regulatory role in myocardial infarction through various mechanisms including apoptosis, inflammation, and structural remodeling, highlighting their potential as therapeutic targets and diagnostic biomarkers.
miRNAs may modulate post-MI remodeling; leaves open therapeutic targeting pending prospective trials.
Myocardial infarction (MI) is the most frequent end-point of cardiovascular pathology, leading to higher mortality worldwide. Due to the particularity of the heart tissue, patients who experience ischemic infarction of the heart, still suffered irreversible damage to the heart even if the vascular reflow by treatment, and severe ones can lead to heart failure or even death. In recent years, several studies have shown that microRNAs (miRNAs), playing a regulatory role in damaged hearts, bring light for patients to alleviate MI. In this review, we summarized the effect of miRNAs on MI with some mechanisms, such as apoptosis, autophagy, proliferation, inflammatory; the regulation of miRNAs on cardiac structural changes after MI, including angiogenesis, myocardial remodeling, fibrosis; the application of miRNAs in stem cell therapy and clinical diagnosis; other non-coding RNAs related to miRNAs in MI during the past 5 years.
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Wu et al. (2022) conducted a review in Myocardial infarction. MicroRNAs was evaluated. MicroRNAs regulate myocardial infarction through apoptosis, autophagy, proliferation, and inflammation, offering potential applications in stem cell therapy and clinical diagnosis.
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