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This editorial refers to ‘Aspirin treatment hampers the use of plasma microRNA-126 as a biomarker for the progression of vascular disease’[†][1], by H.C. de Boer et al ., on page 3451 MicroRNAs (miRNAs) have been proven to be key regulators of the cardiovascular system, orchestrating physiological development, inflammation, hypertrophy, ischaemia/reperfusion injury, angiogenesis, atherosclerosis, apoptosis, and fibrosis.1 In addition to their presence within cells, miRNAs can be found in the bloodstream because, in contrast to naked RNA, circulating miRNAs are highly resistant to RNase degradation on account of (i) their transport in exosomes, apoptotic bodies, or microparticles; (ii) their association with lipoprotein complexes, such as HDL; or (iii) their binding to protein complexes, such as the Argonaute family or nucleophosmin.2 Different tissues contribute to the circulating pool of miRNAs, with a significant percentage probably originating from blood and inflammatory cells. Interestingly, the levels of circulating miRNAs have been found to be altered in pathologies such as acute myocardial infarction (AMI),3 heart failure,4 coronary artery disease (CAD),5 and type 2 diabetes mellitus (T2DM).6 This occurs, for example, because cell damage, such as the necrosis of cardiomyocytes in AMI, causes the release of cellular miRNAs into the bloodstream: in fact, cardiac-specific miRNAs (such as miR-1, miR-133a, and miR-208b) are found to be elevated in blood after AMI, correlating well with troponin T serum levels.7 Extracellular miRNAs, therefore, are gaining interest because of their potential as biomarkers. Currently, however, their use as diagnostic biomarkers is still limited,8 with … [1]: #fn-2

Platelets, endothelium, and circulating microRNA-126 as a prognostic biomarker in cardiovascular diseases: per aspirin ad astra