ArticleNature cardiovascular research2023
The VE-cadherin/AmotL2 mechanosensory pathway suppresses aortic inflammation and the formation of abdominal aortic aneurysms.
Article in Nature cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Emerging Mechanisms of Abdominal Aortic Aneurysm.Current atherosclerosis reports · 2026Review
- Article
- Olfactory Receptors and Aortic Aneurysm: Review of Disease Pathways.Journal of clinical medicine · 2024Review
- A phenotypic screening approach to target p60AmotL2-expressing invasive cancer cells.Journal of experimental & clinical cancer research : CR · 2024Article
- Regulation of YAP Promotor Accessibility in Endothelial Mechanotransduction.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Shear Stress and Endothelial Mechanotransduction in Trauma Patients with Hemorrhagic Shock: Hidden Coagulopathy Pathways and Novel Therapeutic Strategies.International journal of molecular sciences · 2023Review
- Nuclear mechanosensing of the aortic endothelium in health and disease.Disease models & mechanisms · 2023Review
- Modulation of E-Cadherin Function through the AmotL2 Isoforms Promotes Ameboid Cell Invasion.Cells · 2023Article
- Atherosclerosis and endothelial mechanotransduction: current knowledge and models for future research.American journal of physiology. Cell physiology · 2023Review
- Endothelial dysfunction in Marfan syndrome mice is restored by resveratrol.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Endothelial cells respond to mechanical forces exerted by blood flow. Endothelial cell-cell junctions and the sites of endothelial adhesion to the matrix sense and transmit mechanical forces to the cellular cytoskeleton. Here we show that the scaffold protein AmotL2 connects junctional VE-cadherin and actin filaments to the nuclear lamina. AmotL2 is essential for the formation of radial actin filaments and the alignment of endothelial cells, and, in its absence, nuclear integrity and positioning are altered. Molecular analysis demonstrated that VE-cadherin binds to AmotL2 and actin, resulting in a cascade that transmits extracellular mechanical signals to the nuclear membrane. Furthermore, the endothelial deficit of AmotL2 in mice fed normal diet provoked a pro-inflammatory response and abdominal aortic aneurysms (AAAs). Transcriptome analysis of human AAA samples revealed a negative correlation between AmotL2 and inflammation of the aortic intima. These findings offer insight into the link between junctional mechanotransduction and vascular disease.
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Registered trials
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