ArticleScientific reports2021
High intraluminal pressure promotes vascular inflammation via caveolin-1.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Role of Caveolin-1 in Inflammation: Genetic Predisposition and Potential Implication for Multiple Sclerosis.Genes · 2026Review
- Caveolin-1 levels associated with coronary artery disease in Chinese participants: a retrospective cohort study.Frontiers in cardiovascular medicine · 2026Article
- Neuroimmune Interactions and Their Role in Immune Cell Trafficking in Cardiovascular Diseases and Cancer.International journal of molecular sciences · 2025Review
- Caveolin and oxidative stress in cardiac pathology.Frontiers in physiology · 2025Review
- Review
- Caveolin-1: A Review of Intracellular Functions, Tissue-Specific Roles, and Epithelial Tight Junction Regulation.Biology · 2023Review
- Physiological functions of caveolae in endothelium.Current opinion in physiology · 2023Article
- Role of Caveolin-1 in Sepsis - A Mini-Review.Frontiers in immunology · 2022Review
- Diversity of Lipid Function in Atherogenesis: A Focus on Endothelial Mechanobiology.International journal of molecular sciences · 2021Review
- The Transient Receptor Potential Vanilloid 4 Channel and Cardiovascular Disease Risk Factors.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aetiology and progression of hypertension involves various endogenous systems, such as the renin angiotensin system, the sympathetic nervous system, and endothelial dysfunction. Recent data suggest that vascular inflammation may also play a key role in the pathogenesis of hypertension. This study sought to determine whether high intraluminal pressure results in vascular inflammation. Leukocyte adhesion was assessed in rat carotid arteries exposed to 1 h of high intraluminal pressure. The effect of intraluminal pressure on signaling mechanisms including reactive oxygen species production (ROS), arginase expression, and NFĸB translocation was monitored. 1 h exposure to high intraluminal pressure (120 mmHg) resulted in increased leukocyte adhesion and inflammatory gene expression in rat carotid arteries. High intraluminal pressure also resulted in a downstream signaling cascade of ROS production, arginase expression, and NFĸB translocation. This process was found to be angiotensin II-independent and mediated by the mechanosensor caveolae, as caveolin-1 (Cav1)-deficient endothelial cells and mice were protected from pressure-induced vascular inflammatory signaling and leukocyte adhesion. Cav1 deficiency also resulted in a reduction in pressure-induced glomerular macrophage infiltration in vivo. These findings demonstrate Cav1 is an important mechanosensor in pressure-induced vascular and renal inflammation.
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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.