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This editorial refers to ‘MicroRNA-1298 is regulated by DNA methylation and affects vascular smooth muscle cell function by targeting connexin 43’ by W. Hu et al. , pp. 534–545. Atherosclerosis constitutes the leading cause of cardiovascular disease resulting in ischaemia of dependent organs due to arterial occlusion. It affects not only heart and brain, but also limbs and other organs with fatal consequences for the individuum. The process invokes profound remodelling of the entire vascular wall driven by inflammation, which affects endothelial cells and promotes the activation of vascular smooth muscle cells (VSMCs). In healthy vessels, VSMCs retain a quiescent, contractile state but in response to environmental cues (chemical and mechanical) they adopt an activated, synthetic state characterized also by proliferation and migration. This remarkable plasticity is achieved through a substantial change in gene expression profile, which is likely governed by epigenetic and/or transcriptional control mechanisms.In addition to transcriptional regulation, non-coding, single-stranded, small RNAs (typically ∼22 nucleotides) contribute substantially to the phenotypic modulation of VSMCs through post-transcriptional regulation of gene expression (mRNA degradation or translational repression).1,2 These so-called microRNAs (miRNAs/miRs) promote or inhibit the switch of VSMCs to the synthetic state. For example, the miR-143/145 cluster supports a contractile state and was down-regulated by vascular injury, implicating that its lack fosters the synthetic state.3,4 Conversely, other miRNAs (miR-21, miR-221/222) were found to promote the synthetic …

Keep calm and carry on: miR-1298 prevents up-regulation of Cx43 and secures a quiescent vascular smooth muscle cell: Figure 1