ArticleJournal of cardiothoracic surgery2026
A potential role of the circ_UBR4/miR-10a-5p/KLF4 axis in regulating vascular smooth muscle cell phenotypic transformation : implications for cardiac allograft vasculopathy.
Article in Journal of cardiothoracic surgery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Cardiac Allograft Vasculopathy (CAV) remains a predominant challenge in post-transplant cardiac care. The phenotypic transformation of vascular smooth muscle cells (VSMCs) is central to its progression, contributing to neointimal hyperplasia and long-term graft failure. Recent studies have highlighted the involvement of non-coding RNAs as essential modulators in VSMC regulation, opening new avenues for therapeutic exploration. In this study, we aimed to explore the role of the circ_UBR4/miR-10a-5p/KLF4 regulatory axis in VSMC phenotypic switching. Human aortic smooth muscle cells (HASMCs) underwent co-transfection with constructed plasmids of both wild-type and mutated sequences for circ_UBR4 and KLF4, along with respective miR-10a-5p mimics or controls. Functional and mechanistic assays, including dual-luciferase reporter analysis, flow cytometry, Transwell migration and invasion assays, qRT-PCR, Western blotting, and immunofluorescence, were utilized to investigate interactions and downstream effects. Our results revealed that circ_UBR4 directly interacts with miR-10a-5p, and its suppression led to attenuated VSMC proliferation and migration. This inhibitory effect was reversed by concurrent miR-10a-5p downregulation, suggesting a functional antagonism. Further analyses demonstrated that miR-10a-5p directly targets KLF4, and its overexpression resulted in decreased proliferative capacity and reduced expression of synthetic and proliferative markers (e.g., OPN, MMP-2, PCNA, and ki-67). These effects were counteracted by KLF4 overexpression. In parallel, contractile marker SM-22α showed opposing trends, further confirming phenotypic transition. Together, these findings suggest that the circ_UBR4/miR-10a-5p/KLF4 axis may play a critical role in regulating VSMC phenotypic plasticity. Insights from this study provide new molecular insights that could inform our understanding of CAV pathogenesis and may represent potential targets for future therapeutic exploration in transplant cardiology.
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