ArticleArteriosclerosis, thrombosis, and vascular biology2011
RhoA-mediated signaling in Notch-induced senescence-like growth arrest and endothelial barrier dysfunction.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 78 citations in OpenAlex.
- Multivariable genome-wide analysis elucidates the shared genetic architecture, immunosenescence features, and gut-origin therapeutic targets of ulcerative colitis-associated multisystem inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The role of aging on endothelial cell-cell junctions and pulmonary microvascular permeability in male mice.Physiological reports · 2025Article
- ROS-degradable hydrogel delivering LOXL2-LNPs rescues disc degeneration by synchronously suppressing cellular senescence and oxidative damage.Journal of nanobiotechnology · 2025Article
- Matrix stiffness induces endothelial network senescence.bioRxiv : the preprint server for biology · 2025Article
- The role of senescence-related genes in major depressive disorder: insights from machine learning and single cell analysis.BMC psychiatry · 2025Article
- Exendin-4 Reduces Senescence of Inflammation-Induced Periodontal Ligament Stem Cells Through SIRT1/Notch1 Signaling.Stem cells international · 2025Article
- Blood vessel organoids generated by base editing and harboring single nucleotide variation in Notch3 effectively recapitulate CADASIL-related pathogenesis.Molecular neurobiology · 2024Article
- Review
- Transient low shear-stress preconditioning influences long-term endothelial traction and alignment under high shear flow.American journal of physiology. Heart and circulatory physiology · 2024Article
- Aging in Ocular Blood Vessels: Molecular Insights and the Role of Oxidative Stress.Biomedicines · 2024Review
- MYL3 protects chondrocytes from senescence by inhibiting clathrin-mediated endocytosis and activating of Notch signaling.Nature communications · 2023Article
- Review
- Notch Signaling in the Vasculature: Angiogenesis and Angiocrine Functions.Cold Spring Harbor perspectives in medicine · 2023Review
- Premature senescence of the liver in Alagille patients.PloS one · 2023Article
- Hedgehog signaling is controlled by Rac1 activity.Theranostics · 2022Article
- Dynamic Crosstalk between Vascular Smooth Muscle Cells and the Aged Extracellular Matrix.International journal of molecular sciences · 2021Review
- CADASIL from Bench to Bedside: Disease Models and Novel Therapeutic Approaches.Molecular neurobiology · 2021Review
- Endothelial sprouting, proliferation, or senescence: tipping the balance from physiology to pathology.Cellular and molecular life sciences : CMLS · 2021Review
- Effect of Active Ingredients of Chinese Herbal Medicine on the Rejuvenation of Healthy Aging: Focus on Stem Cells.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- Notch3 Modulates Cardiac Fibroblast Proliferation, Apoptosis, and Fibroblast to Myofibroblast Transition via Negative Regulation of the RhoA/ROCK/Hif1α Axis.Frontiers in physiology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveNotch signaling has a critical role in vascular development and morphogenesis. Activation of Notch in endothelial cells led to a senescence-like phenotype with loss of barrier function. Our objective was to understand the molecular pathways mediating this phenotype. METHODS AND
resultsHuman primary endothelial cells increase expression of Notch receptors and ligands during propagation in vitro toward natural senescence. This senescence was induced at low passage with Notch activation. We characterized the pathways activated downstream of Notch signaling. Notch was activated by Delta-like 4 ligand or constitutively active Notch receptors and measured for cell proliferation, migration, and sprouting. Notch signaling triggered early senescence in low-passage cells, characterized by increased p53 and p21 expression. The senescence phenotype was associated with hyperpermeability of the monolayer, with disrupted vascular endothelial cadherin and β-catenin levels and localization. Consistent with changes in cell shape and contact, we demonstrated that Notch activation increases myosin light chain phosphorylation by activating Rho kinase. Inhibition of Rho abrogated Notch-induced myosin light chain phosphorylation and led to enhanced barrier function by reorganizing F-actin to β-catenin-containing cell-cell adherens junctions.
conclusionsOur findings show that RhoA/Rho kinase regulation by Notch signaling in endothelial cells triggers a senescence phenotype associated with endothelial barrier dysfunction.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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 OpenQuestion graph.