Although left atrial (LA) function is of major clinical importance in cardiovascular diseases, traditional indicators such as LA volume struggle to promptly reflect functional changes. In recent years, the emerging technique of left atrial strain (LAS) has garnered widespread attention. As a quantitative metric based on speckle tracking echocardiography, LAS can detect subtle functional abnormalities in the LA myocardium at an early stage and independently assess atrial reservoir, conduit, and contraction functions beyond volume changes. Numerous recent studies have demonstrated the significant clinical utility of LAS across multiple cardiovascular conditions, including heart failure, atrial fibrillation, hypertension, valvular heart disease, and coronary artery disease. Furthermore, LAS exhibits prognostic value in cardiomyopathies and cancer therapy–related cardiotoxicity. This review summarizes recent advances in LAS across various cardiovascular diseases, objectively evaluates its clinical application prospects and limitations, and outlines future research directions.
Jia-Jun Chen, Guo-Xing Ling, Chen Fang et al.· Reviews in cardiovascular me...· 0 citations
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.
Haoqiu Zhong, Zhanyu Xu, Mingyao Zhou et al.· Journal of Cardiothoracic Su...· 0 citations
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