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Background: Long non-coding RNAs (LncRNAs) play important roles in doxorubicin (DOX)-induced apoptosis of cardiomyocytes. However, the function of lncRNA SOX2-OT is unclear. This study was carried out to investigate the function of SOX2-OT in doxorubicin-induced cardiomyocyte apoptosis.
Methods: qRT-PCR and immunoblotting were used to detect the expression levels of SOX2-OT, miR-942-5p and death protein-5 (DP5) in DOX-treated primary cardiomyocytes and rat models. The relationship among miR-942-5p, SOX2-OT, and DP5 was explored by luciferase reporter assay. The effects of SOX2-OT, miR-942-5p and DP5 on doxorubicin-induced cardiomyocyte apoptosis were evaluated by Annexin V-FITC/PI method and caspase-3 activity assay. The effect of SOX2-OT on cardiomyocyte apoptosis was analyzed by TUNEL staining and echocardiography.
Results: SOX2-OT and DP5 were highly expressed, while miR-942-5p was down-regulated in DOX-treated primary cardiomyocytes and rat model. SOX2-OT can upregulate DP5 as a sponge of miR-942-5p, which was a direct target of miR-942-5p. In addition, miR-942-5p reversed the protective effect of knockdown of SOX2-OT on cardiomyocytes by inhibiting the expression of DP5 in vitro and in vivo.
Conclusion: Knockdown of SOX2-OT down-regulated DP5 via sponging miR-942-5p and inhibiting DOX-induced apoptosis of primary cardiomyocytes.
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http://dx.doi.org/10.2147/DDDT.S267474 | DOI Listing |
Am J Physiol Heart Circ Physiol
September 2025
Division of Pediatric Critical Care, Department of Pediatrics, University of California, San Francisco, USA.
Right ventricular (RV) failure is the primary cause of death among patients with pulmonary arterial hypertension (PAH). Patients with congenital heart disease-associated PAH (CHD-PAH) demonstrate improved outcomes compared to patients with other forms of PAH, which is related to the maintenance of an adaptively hypertrophied RV. In an ovine model of CHD-PAH, we aimed to elucidate the cellular, microvascular, and transcriptional adaptations to congenital pressure overload that support RV function.
View Article and Find Full Text PDFJTCVS Open
August 2025
Division of Congenital Heart Surgery, Department of Surgery, Texas Children's Hospital Heart Center and Baylor College of Medicine, Houston, Tex.
Objective: Pediatric pulmonary vein stenosis (PVS) is associated with substantial morbidity and mortality for the subset of patients with recurrent or progressive disease. The molecular mechanisms underlying the development and trajectory of PVS remain unclear. This study characterizes the transcriptome of clinical and phenotypic subtypes of PVS.
View Article and Find Full Text PDFCardiovasc Ther
September 2025
Department of Cardiac Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yes-associated protein (YAP) is a major downstream nuclear coactivator of the Hippo pathway and is activated during myocardial hypertrophy. Verteporfin, a YAP inhibitor, may serve as a potential treatment for myocardial hypertrophy. This study was aimed at exploring the role and underlying mechanisms of verteporfin in isoproterenol (ISO)-induced myocardial hypertrophy both in vivo and in vitro.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Department of Chemical and Biomolecular Engineering, Samueli School of Engineering, University of California, Irvine, CA 92697.
Charge and energy transport within living systems are fundamental processes that enable the autonomous function of excitable cells and tissues. To date, localized control of these transport processes has been enabled by genetic modification approaches to render light sensitivity to cells. Here, we present peptidic nanoassemblies as constituents of a cardiac biomaterial platform that leverages complementary sequence interactions to direct photoinduced energy transport at the cellular interface.
View Article and Find Full Text PDFAdv Healthc Mater
September 2025
Singapore Centre for 3D Printing, Nanyang Technological University, Singapore, 639798, Singapore.
Organotypic 3D tissue models require precise electrophysiological interfaces to study function and disease. Multi-electrode arrays (MEAs) are essential for recording and stimulation, yet conventional fabrication methods are costly and time-intensive. This study demonstrates aerosol jet printing (AJP) of gold nanoparticles onto flexible polyimide substrates to produce fully gold, biocompatible MEAs for rapid customization of MEAs.
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