ArticleClinical science (London, England : 1979)2014
Caveolin 1 is critical for abdominal aortic aneurysm formation induced by angiotensin II and inhibition of lysyl oxidase.
Article in Clinical science (London, England : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Integrated Network and Transcriptomic Analyses Identify a Candidate Ethanol-ADAM17 Molecular Axis Associated with Glioblastoma Progression.International journal of molecular sciences · 2026Article
- Genetic Manipulation of Caveolin-1 in a Transgenic Mouse Model of Aortic Root Aneurysm: Sex-Dependent Effects on Endothelial and Smooth Muscle Function.International journal of molecular sciences · 2024Article
- Endoplasmic reticulum stress in abdominal aortic aneurysm.International journal of cardiology. Heart & vasculature · 2024Review
- β-Aminopropionitrile Induces Distinct Pathologies in the Ascending and Descending Thoracic Aortic Regions of Mice.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- β-aminopropionitrile Induces Distinct Pathologies in the Ascending and Descending Thoracic Aortic Regions of Mice.bioRxiv : the preprint server for biology · 2024Article
- Mitochondrial fission inhibition protects against hypertension induced by angiotensin II.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Identification of abdominal aortic aneurysm subtypes based on mechanosensitive genes.PloS one · 2024Article
- Vascular dysfunction in COVID-19 patients: update on SARS-CoV-2 infection of endothelial cells and the role of long non-coding RNAs.Clinical science (London, England : 1979) · 2022Article
- Progress in murine models of ruptured abdominal aortic aneurysm.Frontiers in cardiovascular medicine · 2022Review
- Contribution of ADAM17 and related ADAMs in cardiovascular diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Testosterone Metabolite 6β-Hydroxytestosterone Contributes to Angiotensin II-Induced Abdominal Aortic Aneurysms inJournal of the American Heart Association · 2021Article
- Targeting mitochondrial fission as a potential therapeutic for abdominal aortic aneurysm.Cardiovascular research · 2021Article
- Lysyl Oxidase (LOX): Functional Contributions to Signaling Pathways.Biomolecules · 2020Review
- MMPs and ADAMs/ADAMTS inhibition therapy of abdominal aortic aneurysm.Life sciences · 2020Review
- Potential Molecular Pathways Related to Pulmonary Artery Aneurysm Development: Lessons to Learn from the Aorta.International journal of molecular sciences · 2020Review
- Stimulation of Caveolin-1 Signaling Improves Arteriovenous Fistula Patency.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Inhibition of endoplasmic reticulum stress by intermedin1-53 attenuates angiotensin II-induced abdominal aortic aneurysm in ApoE KO Mice.Endocrine · 2018Article
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- Understanding Angiotensin II Type 1 Receptor Signaling in Vascular Pathophysiology.Hypertension (Dallas, Tex. : 1979) · 2018Review
- Vascular ADAM17 (a Disintegrin and Metalloproteinase Domain 17) Is Required for Angiotensin II/β-Aminopropionitrile-Induced Abdominal Aortic Aneurysm.Hypertension (Dallas, Tex. : 1979) · 2017Article
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9 authors.
Funding
Abstract
Although AngII (angiotensin II) and its receptor AT1R (AngII type 1 receptor) have been implicated in AAA (abdominal aortic aneurysm) formation, the proximal signalling events primarily responsible for AAA formation remain uncertain. Caveolae are cholesterol-rich membrane microdomains that serve as a signalling platform to facilitate the temporal and spatial localization of signal transduction events, including those stimulated by AngII. Cav1 (caveolin 1)-enriched caveolae in vascular smooth muscle cells mediate ADAM17 (a disintegrin and metalloproteinase 17)-dependent EGFR (epidermal growth factor receptor) transactivation, which is linked to vascular remodelling induced by AngII. In the present study, we have tested our hypothesis that Cav1 plays a critical role for the development of AAA at least in part via its specific alteration of AngII signalling within caveolae. Cav1-/- mice and the control wild-type mice were co-infused with AngII and β-aminopropionitrile to induce AAA. We found that Cav1-/- mice with the co-infusion did not develop AAA compared with control mice in spite of hypertension. We found an increased expression of ADAM17 and enhanced phosphorylation of EGFR in AAA. These events were markedly attenuated in Cav1-/- aortas with the co-infusion. Furthermore, aortas from Cav1-/- mice with the co-infusion showed less endoplasmic reticulum stress, oxidative stress and inflammatory responses compared with aortas from control mice. Cav1 silencing in cultured vascular smooth muscle cells prevented AngII-induced ADAM17 induction and activation. In conclusion, Cav1 appears to play a critical role in the formation of AAA and associated endoplasmic reticulum/oxidative stress, presumably through the regulation of caveolae compartmentalized signals induced by AngII.
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