LncRNA HULC-miR-556-5p axis regulates cardiac microvascular endothelial cell function in chronic heart failure through the AMPK/FOXO3 pathway

Purpose This study aimed to investigate the regulatory mechanism of miR-556-5p in endothelial cell injury associated with heart failure and its impact on endothelial cell function. Methods Human cardiac microvascular endothelial cells (HCMECs) were utilized as the study model. The expression levels of miR-556-5p and related proteins were assessed using techniques such as real-time quantitative PCR and Western blot. Cell apoptosis detection, analysis of inflammatory cytokine release, cell viability assays, and immunoblotting were employed to evaluate cell function and physiological status. Results We observed a crucial role of miR-556-5p in Ang II-induced HCMEC injury. Upregulation of miR-556-5p significantly suppressed cell apoptosis and the release of inflammatory cytokines (such as TNF-α, IL-1β, and IL-6), while promoting cell survival. Further experimental results indicated that miR-556-5p regulated cell function by reducing the expression level of FOXO3 and possibly modulating the AMPK signaling pathway to affect the physiological status of endothelial cells. Additionally, miR-556-5p markedly decreased cellular autophagy levels, further supporting its regulatory role in endothelial cell injury associated with heart failure. Conclusion This study elucidates the important role of miR-556-5p in endothelial cell injury associated with heart failure, providing new insights into the pathophysiological mechanisms of heart failure.