ArticleAmerican journal of physiology. Heart and circulatory physiology2015
Differences in genetic signaling, and not mechanical properties of the wall, are linked to ascending aortic aneurysms in fibulin-4 knockout mice.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Transport across the thoracic aortic wall: implications for aneurysm pathobiology, diagnosis, and treatment.American journal of physiology. Heart and circulatory physiology · 2025Review
- Single-Cell Analyses Offer Insights into the Different Remodeling Programs of Arteries and Veins.Cells · 2024Article
- Changes of collagen content in lung tissues of plateau yak and its mechanism of adaptation to hypoxia.PeerJ · 2024Article
- Experimental and Mouse-Specific Computational Models of the Fbln4Cardiovascular engineering and technology · 2022Article
- Soft-Tissue Material Properties and Mechanogenetics during Cardiovascular Development.Journal of cardiovascular development and disease · 2022Review
- Passive biaxial mechanical behavior of newborn mouse aorta with and without elastin.Journal of the mechanical behavior of biomedical materials · 2022Article
- Captopril treatment during development alleviates mechanically induced aortic remodeling in newborn elastin knockout mice.Biomechanics and modeling in mechanobiology · 2020Article
- Elastic fibers and biomechanics of the aorta: Insights from mouse studies.Matrix biology : journal of the International Society for Matrix Biology · 2020Review
- Comparative gene array analyses of severe elastic fiber defects in late embryonic and newborn mouse aorta.Physiological genomics · 2018Article
- Bio-chemo-mechanics of thoracic aortic aneurysms.Current opinion in biomedical engineering · 2018Article
- Vascular Deformation Mapping (VDM) of Thoracic Aortic Enlargement in Aneurysmal Disease and Dissection.Tomography (Ann Arbor, Mich.) · 2017Article
- Crosslinked elastic fibers are necessary for low energy loss in the ascending aorta.Journal of biomechanics · 2017Article
- Mechanical behavior and matrisome gene expression in the aneurysm-prone thoracic aorta of newborn lysyl oxidase knockout mice.American journal of physiology. Heart and circulatory physiology · 2017Article
- Function of Ltbp-4L and fibulin-4 in survival and elastogenesis in mice.Disease models & mechanisms · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Fibulin-4 is an extracellular matrix protein that is essential for proper assembly of arterial elastic fibers. Mutations in fibulin-4 cause cutis laxa with thoracic aortic aneurysms (TAAs). Sixty percent of TAAs occur in the ascending aorta (AA). Newborn mice lacking fibulin-4 (Fbln4(-/-)) have aneurysms in the AA, but narrowing in the descending aorta (DA), and are a unique model to investigate locational differences in aneurysm susceptibility. We measured mechanical behavior and gene expression of AA and DA segments in newborn Fbln4(-/-) and Fbln4(+/+) mice. Fbln4(-/-) AA has increased diameters compared with Fbln4(+/+) AA and Fbln4(-/-) DA at most applied pressures, confirming genotypic and locational specificity of the aneurysm phenotype. When diameter compliance and tangent modulus were calculated from the mechanical data, we found few significant differences between genotypes, suggesting that the mechanical response to incremental diameter changes is similar, despite the fragmented elastic fibers in Fbln4(-/-) aortas. Fbln4(-/-) aortas showed a trend toward increased circumferential stretch, which may be transmitted to smooth muscle cells (SMCs) in the wall. Gene expression data suggest activation of pathways for SMC proliferation and inflammation in Fbln4(-/-) aortas compared with Fbln4(+/+). Additional genes in both pathways, as well as matrix metalloprotease-8 (Mmp8), are upregulated specifically in Fbln4(-/-) AA compared with Fbln4(+/+) AA and Fbln4(-/-) DA. Mmp8 is a neutrophil collagenase that targets type 1 collagen, and upregulation may be necessary to allow diameter expansion in Fbln4(-/-) AA. Our results provide molecular and mechanical targets for further investigation in aneurysm pathogenesis.
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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.