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

mTOR (Mechanistic Target of Rapamycin) Inhibition Decreases Mechanosignaling, Collagen Accumulation, and Stiffening of the Thoracic Aorta in Elastin-Deficient Mice.

Arteriosclerosis, thrombosis, and vascular biology - 1 Sept 2017

Jiao Yang, Li Guangxin, Li Qingle, Ali Rahmat, Qin Lingfeng, Li Wei, Qyang Yibing, Greif Daniel M, Geirsson Arnar, Humphrey Jay D, Tellides George

Abstract excerpt

OBJECTIVE: Elastin deficiency because of heterozygous loss of an ELN allele in Williams syndrome causes obstructive aortopathy characterized by medial thickening and fibrosis and consequent aortic stiffening. Previous work in Eln-null mice with a severe arterial phenotype showed that inhibition of mTOR (mechanistic target of rapamycin), a key regulator of cell growth, lessened the aortic obstruction but did not...

Read the complete abstract on PubMed

Topics

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

Share to Aorta, Thoracic
Share to Elastin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Everolimus

Share to Focal Adhesion Kinase 1

Share to Mechanistic Target of Rapamycin Complex 1

Share to Mechanistic Target of Rapamycin Complex 2

Share to Vascular Stiffness

Share to Williams Syndrome

Source

Open in PubMed Open full text

Identifiers

PMID: 28751568
DOI: 10.1161/ATVBAHA.117.309653
PMCID: PMC5574180

Genes

ELN

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

mTOR (Mechanistic Target of Rapamycin) Inhibition Decreases Mechanosignaling, Collagen Accumulation, and Stiffening of the Thoracic Aorta in Elastin-Deficient Mice.PMID 28751568Read ↗

Deficient Circumferential Growth Is the Primary Determinant of Aortic Obstruction Attributable to Partial Elastin Deficiency.Semantic proximity Read ↗

Thoracic aortic disease in tuberous sclerosis complex: molecular pathogenesis and potential therapies in Tsc2+/- mice.Semantic proximity Read ↗

Inhibition of the mTOR pathway in abdominal aortic aneurysm: implications of smooth muscle cell contractile phenotype, inflammation, and aneurysm expansion.Semantic proximity Read ↗

Everolimus Rescues the Phenotype of Elastin Insufficiency in Patient Induced Pluripotent Stem Cell-Derived Vascular Smooth Muscle Cells.Semantic proximity Read ↗

Rapamycin reverses hypertrophic cardiomyopathy in a mouse model of LEOPARD syndrome-associated PTPN11 mutation.Semantic proximity Read ↗

Modeling and rescue of the vascular phenotype of Williams-Beuren syndrome in patient induced pluripotent stem cells.Semantic proximity Read ↗

A critical role for elastin signaling in vascular morphogenesis and disease.Semantic proximity Read ↗

mTOR Inhibition Prolongs Survival and Has Beneficial Effects on Heart Function After Onset of Lamin A/C Gene Mutation Cardiomyopathy in Mice.Semantic proximity Read ↗

Integrin β3 inhibition is a therapeutic strategy for supravalvular aortic stenosis.Semantic proximity Read ↗

Pharmacologically Improved Contractility Protects Against Aortic Dissection in Mice With Disrupted Transforming Growth Factor-β Signaling Despite Compromised Extracellular Matrix Properties.Semantic proximity Read ↗

mTOR signaling controls the formation of smooth muscle cell-derived intimal fibroblasts during vasculitisSemantic proximity Read ↗

Hyperactive mTORC1 in lung mesenchyme induces endothelial cell dysfunction and pulmonary vascular remodelingSemantic proximity Read ↗

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