MicroRNAs in Acute ST Elevation Myocardial Infarction—A New Tool for Diagnosis and Prognosis: Therapeutic Implications

Abstract

Despite diagnostic and therapeutic advances, coronary artery disease and especially its extreme manifestation, ST elevation myocardial infarction (STEMI), remain the leading causes of morbidity and mortality worldwide. Early and prompt diagnosis is of great importance regarding the prognosis of STEMI patients. In recent years, microRNAs (miRNAs) have emerged as promising tools involved in many pathophysiological processes in various fields, including cardiovascular diseases. In acute coronary syndromes (ACS), circulating levels of miRNAs are significantly elevated, as an indicator of cardiac damage, making them a promising marker for early diagnosis of myocardial infarction. They also have prognostic value and great potential as therapeutic targets considering their key function in gene regulation. This review aims to summarize current information about miRNAs and their role as diagnostic, prognostic and therapeutic targets in STEMI patients.

Current Knowledge of MicroRNAs (miRNAs) in Acute Coronary Syndrome (ACS): ST-Elevation Myocardial Infarction (STEMI)

“…As observed, they detain key functions in cardiac biogenesis, development, and progression, and given their stable structure and rapid circulation release after myocardial injury, they were proposed as potential future biomarkers in ACS. More specifically, older and recent evidence point out the potential role of miRNAs as novel biomarkers not only in STEMI, but also in STEMI's secondary complication such as LVR or HF (Table 1), , or even their use as promising new therapeutic targets [180,181] (Table 2). More than that, miRNAs have the potential to be used in the differential diagnosis of ACS [17,182] with: unstable angina [183], NSTEMI [94,184], and acute myocarditis [185].…”

Cardiac Remodeling After Myocardial Infarction: Functional Contribution of microRNAs to Inflammation and Fibrosis

“…For instance, miR-133a has been shown to have beneficial effects on infarcted hearts by inhibiting inflammation and angiogenesis via FGFR1 and VEGFR2 signaling pathways ( 82 , 83 ). Similarly, miR-320 and miR-144-3p, have been shown to be involved in post-MI responses by regulating PTEN/PI3K/Akt signaling pathway ( 13 , 84 , 85 ); miR-144-3p promotes cardiac fibrosis via targeting PTEN following MI ( 14 ); miR-199a-3p and miR-590-3p also improve cardiac function after MI ( 8 , 86 ); miR-19a/19b inhibits the inflammatory response and has been shown to enhance cardiac function post-MI by targeting Bim1 and PTEN ( 8 ). All these results are relevant when considering that in vivo studies carried out in infarcted mice revealed that angiogenesis can be improved by inhibiting PTEN via activating the PI3K/Akt/VEGF pathway ( 13 , 87 , 88 ).…”

Relationship of Diabetes Mellitus (DM) and Ischemic Heart Disease: Review Article

“…The nature of the hyperglycemic damage in patients affected by DM lies in the accumulation of superoxide anions, which are free radicals capable of activating cellular pathways that includes advanced glycation end products (AGEs), polyol and hexosamine flux, PKC, and vascular inflammation mediated by nuclear factor-B. Hyperglycemia itself also increases oxidative stress through greater glucose oxidation in the citric acid cycle (14) . All these different hyperglycemia consequences lead to decreased cellular resistance to oxidative stress, amplification of the proinflammatory response, and apoptosis of endothelial cells and their overall dysfunction.…”