ArticleEuropean heart journal2023
Vinculin phosphorylation impairs vascular endothelial junctions promoting atherosclerosis.
Article in European heart journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
- S-Adenosylmethionine-Dependent Methylation, Protein Arginine Methyltransferases and Cardiovascular Diseases.Biomolecules · 2026Review
- CNN3 promotes vascular smooth muscle cells proliferation and migration to deteriorate atherosclerosis by β-catenin signaling pathway.Atherosclerosis plus · 2026Article
- HSP27 regulates force-coordinated DDR1 condensate disassembly and liquid-to-gel phase transition.Science advances · 2026Article
- INO80E Suppresses Oxidized LDL-Induced Endothelial Apoptosis Through HDAC1-Mediated Stabilization of YY1.Biomolecules · 2026Article
- Phosphoproteomics in Vascular Biology and Disease: Illuminating Signaling in the Vessel.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Vascular mechanical forces and vascular diseases.Journal of advanced research · 2026Review
- NCKAP1 coordinates focal adhesion and adherens junction dynamics in endothelial barrier maintenance and angiogenesis.iScience · 2026Article
- Pro-Inflammatory Activation Promotes Atherogenic Endothelial Phenotype in Male and Female Human Umbilical Endothelial Vein Cells (HUVECs).International journal of molecular sciences · 2026Article
- Synergistic fusion of CD47, VE-cadherin and mussel adhesion protein promotes endothelialization and suppresses inflammation in vascular stents.Bioactive materials · 2026Article
- Talin1 modulates the Piezo1-YAP axis to regulate endothelial cell inflammation and atherosclerosis.Cellular and molecular life sciences : CMLS · 2025Article
- Review
- Vinculin Y822 phosphorylation regulates adhesion remodeling during cardiomyocyte maturation.Journal of cell science · 2025Article
- The GRK2/AP-1 Signaling Axis Mediates Vascular Endothelial Dysfunction and Atherosclerosis Induced by Oscillatory Low Shear Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The role of cell junctions in atherosclerosis: implications for inflammation, endothelial dysfunction, and plaque stability.Journal of physiology and biochemistry · 2025Review
- Identification of Schwann Cells in Human Intracranial Arteries: Potential Regulatory Role in Atherosclerotic Plaque Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Investigating the role of gut microbiota in diabetic nephropathy through plasma proteome mediated analysis.Scientific reports · 2025Article
- Facile Synthesis of Designer Shape-Defined Mesoporous Metal Nanoenzymes as Therapeutics for Diseases Involving Excessive Oxidative Stress.Biomaterials research · 2025Article
- Follicular Helper T Cells: Potential Interventional Targets in Atherosclerosis.Journal of immunology research · 2025Review
- Bridging the Gap: Endothelial Dysfunction and the Role of iPSC-Derived Endothelial Cells in Disease Modeling.International journal of molecular sciences · 2024Review
- Plasma exosomes from patients with coronary artery disease promote atherosclerosis via impairing vascular endothelial junctions.Scientific reports · 2024Article
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Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsAtherosclerosis preferentially develops in arterial branches and curvatures where vascular endothelium is exposed to disturbed flow. In this study, the effects of disturbed flow on the regulation of vascular endothelial phosphoproteins and their contribution to therapeutic application in atherogenesis were elucidated.
methodsPorcine models, large-scale phosphoproteomics, transgenic mice, and clinical specimens were used to discover novel site-specific phosphorylation alterations induced by disturbed flow in endothelial cells (ECs).
resultsA large-scale phosphoproteomics analysis of native endothelium from disturbed (athero-susceptible) vs. pulsatile flow (athero-resistant) regions of porcine aortas led to the identification of a novel atherosclerosis-related phosphoprotein vinculin (VCL) with disturbed flow-induced phosphorylation at serine 721 (VCLS721p). The induction of VCLS721p was mediated by G-protein-coupled receptor kinase 2 (GRK2)S29p and resulted in an inactive form of VCL with a closed conformation, leading to the VE-cadherin/catenin complex disruption to enhance endothelial permeability and atherogenesis. The generation of novel apolipoprotein E-deficient (ApoE-/-) mice overexpressing S721-non-phosphorylatable VCL mutant in ECs confirmed the critical role of VCLS721p in promoting atherosclerosis. The administration of a GRK2 inhibitor to ApoE-/- mice suppressed plaque formation by inhibiting endothelial VCLS721p. Studies on clinical specimens from patients with coronary artery disease (CAD) revealed that endothelial VCLS721p is a critical clinicopathological biomarker for atherosclerosis progression and that serum VCLS721p level is a promising biomarker for CAD diagnosis.
conclusionsThe findings of this study indicate that endothelial VCLS721p is a valuable hemodynamic-based target for clinical assessment and treatment of vascular disorders resulting from atherosclerosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.