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

Inactivation of the tumour suppressor, PTEN, in smooth muscle promotes a pro-inflammatory phenotype and enhances neointima formation.

Cardiovascular research - 1 May 2010

Furgeson Seth B, Simpson Peter A, Park Insun, Vanputten Vicki, Horita Henrick, Kontos Christopher D, Nemenoff Raphael A, Weiser-Evans Mary C M

Abstract excerpt

AIMS: Phosphatase and tensin homolog (PTEN) is implicated as a negative regulator of vascular smooth muscle cell (SMC) proliferation and injury-induced vascular remodelling. We tested if selective depletion of PTEN only in SMC is sufficient to promote SMC phenotypic modulation, cytokine productio...

Read the complete abstract on PubMed

Topics

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

Share to Carotid Artery Injuries
Share to Cell Dedifferentiation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Inflammation Mediators

Share to Muscle, Smooth, Vascular

Share to Myocytes, Smooth Muscle

Share to PTEN Phosphohydrolase

Share to TOR Serine-Threonine Kinases

Share to Tunica Intima

Source

Open in PubMed Open full text

Identifiers

PMID: 20051384
DOI: 10.1093/cvr/cvp425
PMCID: PMC2856191

Genes

PTEN
CXCL1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-20051384-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Inactivation of the tumour suppressor, PTEN, in smooth muscle promotes a pro-inflammatory phenotype and enhances neointima formation.PMID 20051384Read ↗

Inhibition of Smooth Muscle β-Catenin Hinders Neointima Formation After Vascular Injury.Semantic proximity Read ↗

Interleukin-1β modulates smooth muscle cell phenotype to a distinct inflammatory state relative to PDGF-DD via NF-κB-dependent mechanisms.Semantic proximity Read ↗

Serum response factor regulates expression of phosphatase and tensin homolog through a microRNA network in vascular smooth muscle cells.Semantic proximity Read ↗

Smooth muscle-selective inhibition of nuclear factor-κB attenuates smooth muscle phenotypic switching and neointima formation following vascular injury.Semantic proximity Read ↗

Conserved miR-370-3p/BMP-7 axis regulates the phenotypic change of human vascular smooth muscle cells.Semantic proximity Read ↗

Smooth muscle hyperplasia due to loss of smooth muscle α-actin is driven by activation of focal adhesion kinase, altered p53 localization and increased levels of platelet-derived growth factor receptor-β.Semantic proximity Read ↗

Lipid phosphate phosphatase 3 negatively regulates smooth muscle cell phenotypic modulation to limit intimal hyperplasia.Semantic proximity Read ↗

The PTEN/PI3K pathway governs normal vascular development and tumor angiogenesis.Semantic proximity Read ↗

Unique, highly proliferative growth phenotype expressed by embryonic and neointimal smooth muscle cells is driven by constitutive Akt, mTOR, and p70S6K signaling and is actively repressed by PTEN.Semantic proximity Read ↗

Opposing Actions of AKT (Protein Kinase B) Isoforms in Vascular Smooth Muscle Injury and Therapeutic Response.Semantic proximity Read ↗

Membrane-Tethered Metalloproteinase Expressed by Vascular Smooth Muscle Cells Limits the Progression of Proliferative Atherosclerotic Lesions.Semantic proximity Read ↗

TGF-β/Smad3 Stimulates Stem Cell/Developmental Gene Expression and Vascular Smooth Muscle Cell De-DifferentiationSemantic proximity Read ↗

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