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

Impaired vascular mechanotransduction in a transgenic mouse model of CADASIL arteriopathy.

Stroke - 1 Jan 2005

Dubroca Caroline, Lacombe Pierre, Domenga Valérie, Maciazek Jacqueline, Levy Bernard, Tournier-Lasserve Elisabeth, Joutel Anne, Henrion Daniel

Abstract excerpt

BACKGROUND AND PURPOSE: CADASIL is an inherited small-vessel disease responsible for lacunar strokes and cognitive impairment. The disease is caused by highly stereotyped mutations in Notch3, the expression of which is highly restricted to vascular smooth muscle cells (VSMCs). The underlying vasc...

Read the complete abstract on PubMed

Topics

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

Share to CADASIL
Share to Phenylephrine
Share to Pressure

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Receptor, Notch3

Share to Receptor, Notch4

Share to Vasoconstriction

Share to Vasoconstrictor Agents

Share to Vasodilation

Source

Open in PubMed Open full text

Identifiers

PMID: 15569862
DOI: 10.1161/01.STR.0000149949.92854.45
PMCID: PMC2234452

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026. Prepared record publication-15569862-2026-09-01.1. Manifest publication-graph-cohort-2026-09-01.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Impaired vascular mechanotransduction in a transgenic mouse model of CADASIL arteriopathy.PMID 15569862Read ↗

CADASILSemantic proximity Read ↗

Transgenic mice expressing mutant Notch3 develop vascular alterations characteristic of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.Semantic proximity Read ↗

Pathogenesis of CADASIL: transgenic and knock-out mice to probe function and dysfunction of the mutated gene, Notch3, in the cerebrovasculature.Semantic proximity Read ↗

Increased Notch3 Activity Mediates Pathological Changes in Structure of Cerebral Arteries.Semantic proximity Read ↗

Impaired cerebral vasoreactivity in a transgenic mouse model of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy arteriopathy.Semantic proximity Read ↗

Hypomorphic Notch 3 alleles link Notch signaling to ischemic cerebral small-vessel disease.Semantic proximity Read ↗

Age-related loss of Notch3 underlies brain vascular contractility deficiencies, glymphatic dysfunction, and neurodegeneration in mice.Semantic proximity Read ↗

Selective vulnerability of cerebral vasculature to <i>NOTCH3</i> variants in small vessel disease and rescue by phosphodiesterase-5 inhibitorSemantic proximity Read ↗

Protein aggregates containing wild-type and mutant NOTCH3 are major drivers of arterial pathology in CADASIL.Semantic proximity Read ↗

The archetypal R90C CADASIL–NOTCH3 mutation retains NOTCH3 function in vivoSemantic proximity Read ↗

ER stress and Rho kinase activation underlie the vasculopathy of CADASIL.Semantic proximity Read ↗

Reducing T imp3 or vitronectin ameliorates disease manifestations in CADASIL miceSemantic proximity Read ↗

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