Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Dysfunction of endothelial and smooth muscle cells in small arteries of a mouse model of Marfan syndrome.

British journal of pharmacology - 1 Nov 2009

Syyong H T, Chung A W Y, Yang H H C, van Breemen C

Abstract excerpt

BACKGROUND AND PURPOSE: Marfan syndrome, a connective tissue disorder caused by mutations in FBN1 encoding fibrillin-1, results in life-threatening complications in the aorta, but little is known about its effects in resistance vasculature. EXPERIMENTAL APPROACH: Second-order mesenteric arteries...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Elasticity
Share to Fibrillins
Share to Nitroprusside

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Phenylephrine

Share to Vasoconstriction

Share to Vasoconstrictor Agents

Share to Vasodilation

Share to Vasodilator Agents

Source

Open in PubMed Open full text

Identifiers

PMID: 19814726
DOI: 10.1111/j.1476-5381.2009.00439.x
PMCID: PMC2795226

Genes

FBN1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-19814726-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Dysfunction of endothelial and smooth muscle cells in small arteries of a mouse model of Marfan syndrome.PMID 19814726Read ↗

Loss of elastic fiber integrity and reduction of vascular smooth muscle contraction resulting from the upregulated activities of matrix metalloproteinase-2 and -9 in the thoracic aortic aneurysm in Marfan syndrome.Semantic proximity Read ↗

The aorta in Marfan syndrome: from molecular mechanisms to mechanobiological dysfunction.Semantic proximity Read ↗

Genetic Manipulation of Caveolin-1 in the Mouse Model of Marfan Syndrome Associated Aortic Root Aneurysm: Effects on Endothelial and Smooth Muscle FunctionSemantic proximity Read ↗

Unraveling the Sex-Dependent Relationship Between Central, Peripheral and Cerebral Arteries Function in a Mouse Model of Marfan Syndrome: Benefits of Exercise Training on Vascular Function and Blood FlowSemantic proximity Read ↗

In vivo phenotypic vascular dysfunction extends beyond the aorta in a mouse model for fibrillin-1 (Fbn1) mutation.Semantic proximity Read ↗

Imbalanced synthesis of cyclooxygenase-derived thromboxane A2 and prostacyclin compromises vasomotor function of the thoracic aorta in Marfan syndrome.Semantic proximity Read ↗

Differential contribution of elastin and fibrillin-1 to the cardiovascular phenotype of a double heterozygous Marfan and Williams-Beuren syndrome mouse modelSemantic proximity Read ↗

Cardiac remodeling in the mouse model of Marfan syndrome develops into two distinctive phenotypes.Semantic proximity Read ↗

Intrinsic cardiomyopathy in Marfan syndrome: results from in-vivo and ex-vivo studies of the Fbn1C1039G/+ model and longitudinal findings in humans.Semantic proximity Read ↗

A Marfan-Associated FBN1 Nonsense Mutation Mouse Model Reveals Adventitial Inflammation During Aneurysm ProgressionSemantic proximity Read ↗

Marfan syndrome: new clues to genotype-phenotype correlations.Semantic proximity Read ↗

Cardiovascular Benefits of Moderate Exercise Training in Marfan Syndrome: Insights From an Animal Model.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.