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Pathological vascular endothelial damage caused by hypoxia is the basis of many vascular-related diseases. However, the role of circular RNA in hypoxic vascular injury is still poorly understood. Here, we found that hypoxia induced AFF1 circular RNA (circAFF1) can activate the SAV1/YAP1 and lead to the dysfunction of vascular endothelial cells. In HUV-EC-C and HBEC-5i cells, circAFF1 was upregulated under CoCl induced hypoxic conditions. The abnormal expression of circAFF1 inhibited the proliferation, tube formation, migration of vascular endothelial cells. The effect of circAFF1 is achieved by the adsorption of miR-516b to release SAV1, which in turn causes the phosphorylation of YAP1. Moreover, we found that the upregulation of circAFF1 in 235 Patients with subarachnoid hemorrhage. Taken together, we clarify the role of circAFF1/miR-516b/SAV1/YAP1 axis in vascular endothelial dysfunction and its potential early diagnostic value of disease caused by hypoxia injury in blood vessels.
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http://dx.doi.org/10.3389/fphys.2020.00899 | DOI Listing |
Stem Cell Rev Rep
September 2025
Paris Cité University, INSERM UMR-S 970, Paris Cardiovascular Research Centre, Paris, France.
Endothelial Colony-Forming Cells (ECFCs) are recognized as key vasculogenic progenitors in humans and serve as valuable liquid biopsies for diagnosing and studying vascular disorders. In a groundbreaking study, Anceschi et al. present a novel, integrative strategy that combines ECFCs loaded with gold nanorods (AuNRs) to enhance tumor radiosensitization through localized hyperthermia.
View Article and Find Full Text PDFMol Syst Biol
September 2025
Department of Medicine, Division of Cardiovascular Medicine, Stanford University, Stanford, CA, USA.
Vascular sites have distinct susceptibility to atherosclerosis and aneurysm, yet the epigenomic and transcriptomic underpinning of vascular site-specific disease risk is largely unknown. Here, we performed single-cell chromatin accessibility (scATACseq) and gene expression profiling (scRNAseq) of mouse vascular tissue from three vascular sites. Through interrogation of epigenomic enhancers and gene regulatory networks, we discovered key regulatory enhancers to not only be cell type, but vascular site-specific.
View Article and Find Full Text PDFNat Commun
September 2025
Institute of Computational Biology, German Research Center for Environmental Health, Helmholtz Zentrum München, Neuherberg, Germany.
Atherosclerosis, a major cause of cardiovascular diseases, is characterized by the buildup of lipids and chronic inflammation in the arteries, leading to plaque formation and potential rupture. Despite recent advances in single-cell transcriptomics (scRNA-seq), the underlying immune mechanisms and transformations in structural cells driving plaque progression remain incompletely defined. Existing datasets often lack comprehensive coverage and consistent annotations, limiting the utility of downstream analyses.
View Article and Find Full Text PDFInt Heart J
September 2025
Department of Cardiovascular Medicine, Tokushima University Graduate School of Biomedical Sciences.
The pharmacological blockade of mineralocorticoid receptors (MR) is a potential therapeutic approach to reduce cardiovascular complications. Recent studies suggest that MR blockers affect several extrarenal tissues, including vascular function. We investigated the effects of a novel non-steroidal selective MR blocker, esaxerenone, on vascular function and atherogenesis.
View Article and Find Full Text PDFBMJ Open
September 2025
Department of Gastroenterology, Hepatology, Infectious Diseases and Intoxication, University Hospital Heidelberg, Heidelberg, Germany.
Introduction: Combined vascular endothelial growth factor/programmed death-ligand 1 blockade through atezolizumab/bevacizumab (A/B) is the current standard of care in advanced hepatocellular carcinoma (HCC). A/B substantially improved objective response rates compared with tyrosine kinase inhibitor sorafenib; however, a majority of patients will still not respond to A/B. Strong scientific rationale and emerging clinical data suggest that faecal microbiota transfer (FMT) may improve antitumour immune response on PD-(L)1 blockade.
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