miR-21, miR-210, miR-34a, and miR-146a/b are up-regulated in human atherosclerotic plaques in the Tampere Vascular Study

miR-21 alters circulating Treg function in vascular disease—hope for restoring immunoregulatory responses in atherosclerosis?

“…Indeed, the cells expressing induced-miR-21 in disease remain unidentified and although Treg numbers decrease with vascular disease, the possibility exists that the remaining cells enhance miR-21 to mediate suppressive effects. Although the current study did not examine miR-21 in Treg in atherosclerotic plaques, miR-21 has been reported to be up-regulated in human plaques (18) and differences in local and peripheral regulatory T-cell function may exist. The authors highlight a previous study which demonstrated that Tregs derived from umbilical cord blood (13), which represented a heterogenous population distinct from those of circulating PBMC, also express miR-21 to promote Treg activity through FoxP3.…”

Apolipoprotein E Epsilon 4 Enhances the Association between the rs2910164 Polymorphism of miR-146a and Risk of Atherosclerotic Cerebral Infarction

“…The current evidence supports the hypothesis that miR-146a operates as an important epigenetic regulator in various pathways involved in atherosclerosis and stroke. Thus, we were prompted to explore the relationship between miR146a and ACI 15,16) . Certain single-nucleotide polymorphisms (SNPs) could influence the function of the target genes and are associated with diseases risk 17) .…”

Involvement of the Renin‐Angiotensin System in Atherosclerosis

“…An increase expression of Gal-3 mRNA in human carotid atherosclerotic plaque tissue may be affected by rare genetic variants of the haplotype block, previously associated with Gal-3 circulating levels [85,86]. Diverse cellular processes in atherosclerosis are affected by microRNAs (miRs) and their expression are often tissue and disease-specific [87,88]. Recently, the prediction algorithms and computational methods were applied to identify novel miRs important in pathogenesis of early and advanced atherosclerosis [89].…”