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hsa-miR-548aq-3p is a primate-specific microRNA belonging to the miR-548 family, characterized by its role as a post-transcriptional regulator of gene expression [1, 9]. It functions by binding to the 3' untranslated regions (UTRs) of target mRNAs, such as BAG3 and components of the Hippo and TGF-beta signaling pathways, thereby inducing mRNA degradation or inhibiting translation [3, 5, 8]. In the context of cardiovascular disease, hsa-miR-548aq-3p acts as an anti-angiogenic factor that suppresses the function of endothelial colony forming cells (ECFCs); its downregulation is a key mechanism by which far infrared radiation (FIR) therapy improves vascular repair [1, 14]. Beyond cardiovascular health, this microRNA is dysregulated in various malignancies, including gallbladder and pancreatic cancers, where it may influence tumor progression and serve as a diagnostic biomarker [2, 6]. Therapeutic strategies targeting hsa-miR-548aq-3p involve the use of synthetic miRNA inhibitors (antagomirs) or mimics to modulate its activity in diseased tissues [1, 14].
Post-transcriptional gene silencing via the RNA-induced silencing complex (RISC), leading to mRNA degradation or translational repression of target genes [5, 8].
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