ArticleScientific reports2022
Caveolin-1 is a primary determinant of endothelial stiffening associated with dyslipidemia, disturbed flow, and ageing.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
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- Endothelial Nucleoporin93 (Nup93) Maintains Vascular Homeostasis via Sun1-Dependent Regulation of RhoA/ROCK Activity.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
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- Nanomechanical Characterization of E-Cigarette-Induced Lung Endothelial Dysfunction: Roles of Cortactin and Mitochondrial Reactive Oxygen Species.International journal of molecular sciences · 2025Article
- Adipocytes are dispensable in shaping the ovarian cancer tumor microenvironment in the omentum.bioRxiv : the preprint server for biology · 2025Article
- The Mechanism and Potential Therapeutic Strategies of Vascular Aging.Aging medicine (Milton (N.S.W)) · 2025Review
- Inflammageing, a targetable pathway for preventing cardiovascular diseases.Cardiovascular research · 2025Review
- SARS-CoV-2 uptake and inflammatory response in senescent endothelial cells are regulated by the BSG/VEGFR2 pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Nitrosation of CD36 Regulates Endothelial Function and Serum Lipids.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- PCSK9 Promotes the Malignancy of Triple-negative Breast Cancer Cells by Reducing Cholesterol Levels at the Plasma Membrane to Activate EGFR and HER3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Caveolae: Metabolic Platforms at the Crossroads of Health and Disease.International journal of molecular sciences · 2025Review
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- TGF-β2 enhances nanoscale cortex stiffness via condensation of cytoskeleton-focal adhesion plaque.Biophysical journal · 2025Article
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- Biomechanics-mediated endocytosis in atherosclerosis.Frontiers in cardiovascular medicine · 2024Review
- Modulation of arterial intima stiffness by disturbed blood flow.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Physiological functions of caveolae in endothelium.Current opinion in physiology · 2023Article
- Caveolin-1 and Atherosclerosis: Regulation of LDLs Fate in Endothelial Cells.International journal of molecular sciences · 2023Review
- Paradigms of endothelial stiffening in cardiovascular disease and vascular aging.Frontiers in physiology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Endothelial stiffness is emerging as a major determinant in endothelial function. Here, we analyzed the role of caveolin-1 (Cav-1) in determining the stiffness of endothelial cells (EC) exposed to oxidized low density lipoprotein (oxLDL) under static and hemodynamic conditions in vitro and of aortic endothelium in vivo in mouse models of dyslipidemia and ageing. Elastic moduli of cultured ECs and of the endothelial monolayer of freshly isolated mouse aortas were measured using atomic force microscopy (AFM). We found that a loss of Cav-1 abrogates the uptake of oxLDL and oxLDL-induced endothelial stiffening, as well as endothelial stiffening induced by disturbed flow (DF), which was also oxLDL dependent. Mechanistically, Cav-1 is required for the expression of CD36 (cluster of differentiation 36) scavenger receptor. Genetic deletion of Cav-1 abrogated endothelial stiffening observed in the DF region of the aortic arch, and induced by a high fat diet (4-6 weeks) and significantly blunted endothelial stiffening that develops with advanced age. This effect was independent of stiffening of the sub-endothelium layer. Additionally, Cav-1 expression significantly increased with age. No differences in elastic modulus were observed between the sexes in advanced aged wild type and Cav-1 knockout mice. Taken together, this study demonstrates that Cav-1 plays a critical role in endothelial stiffening induced by oxLDL in vitro and by dyslipidemia, disturbed flow and ageing in vivo.
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