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

Synthetic retinoid Am80 suppresses smooth muscle phenotypic modulation and in-stent neointima formation by inhibiting KLF5.

Circulation research - 25 Nov 2005

Fujiu Katsuhito, Manabe Ichiro, Ishihara Atsushi, Oishi Yumiko, Iwata Hiroshi, Nishimura Go, Shindo Takayuki, Maemura Koji, Kagechika Hiroyuki, Shudo Koichi, Nagai Ryozo

Abstract excerpt

Modulation of smooth muscle cell (SMC) phenotype plays a central role in neointima formation. We recently demonstrated that Am80, a synthetic retinoic acid receptor alpha-specific agonist, inhibits the activity of the transcription factor KLF5, which is essential for neointima formation after vascular injury. In the present study, we aimed to further analyze the mechanism by which Am80 inhibits KLF5 and the...

Read the complete abstract on PubMed

Topics

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

Share to Benzoates
Share to Kruppel-Like Transcription Factors

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Platelet-Derived Growth Factor

Share to Receptors, Retinoic Acid

Share to Retinoic Acid Receptor alpha

Share to Retinoid X Receptor alpha

Share to Stents

Share to Tunica Intima

Source

Identifiers

PMID: 16224062
DOI: 10.1161/01.RES.0000190613.22565.13

Genes

KLF5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Synthetic retinoid Am80 suppresses smooth muscle phenotypic modulation and in-stent neointima formation by inhibiting KLF5.PMID 16224062Read ↗

miRNA-92a Inhibits the Phenotypic Modulation of Vascular Smooth Muscle Cells and May Help to Prevent In-Stent RestenosisSemantic proximity Read ↗

miRNA‑92a inhibits vascular smooth muscle cell phenotypic modulation and may help prevent in‑stent restenosis.Semantic proximity Read ↗

Retinoic acid regulates arterial smooth muscle cell proliferation and phenotypic features in vivo and in vitro through an RARalpha-dependent signaling pathway.Semantic proximity Read ↗

ALK7 Promotes Vascular Smooth Muscle Cells Phenotypic Modulation by Negative Regulating PPARγ Expression.Semantic proximity Read ↗

Retinoids: versatile biological response modifiers of vascular smooth muscle phenotype.Semantic proximity Read ↗

MicroRNA-15b/16 Attenuates Vascular Neointima Formation by Promoting the Contractile Phenotype of Vascular Smooth Muscle Through Targeting YAP.Semantic proximity Read ↗

Sp1-dependent activation of KLF4 is required for PDGF-BB-induced phenotypic modulation of smooth muscle.Semantic proximity Read ↗

Smooth Muscle-Alpha Actin Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Inhibiting Rac1 Activity.Semantic proximity Read ↗

Fluvastatin prevents vascular hyperplasia by inhibiting phenotype modulation and proliferation through extracellular signal-regulated kinase 1 and 2 and p38 mitogen-activated protein kinase inactivation in organ-cultured artery.Semantic proximity Read ↗

Dominant-negative loss of PPARgamma function enhances smooth muscle cell proliferation, migration, and vascular remodeling.Semantic proximity Read ↗

Human activin-A is expressed in the atherosclerotic lesion and promotes the contractile phenotype of smooth muscle cells.Semantic proximity Read ↗

PDGF-DD, a novel mediator of smooth muscle cell phenotypic modulation, is upregulated in endothelial cells exposed to atherosclerosis-prone flow patterns.Semantic proximity Read ↗

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