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

Basal ATP release signals through the P2Y2 receptor to maintain the differentiated phenotype of vascular smooth muscle cells.

Atherosclerosis - 1 Aug 2024

Chen Xingjuan, Obukhov Alexander G, Weisman Gary A, Seye Cheikh I

Abstract excerpt

BACKGROUND AND AIMS: Vascular smooth muscle cell (VSMC) dedifferentiation contributes substantively to vascular disease. VSMCs spontaneously release low levels of ATP that modulate vessel contractility, but it is unclear if autocrine ATP signaling in VSMCs is critical to the maintenance of the VSMC contractile phenotype. METHODS: We used pharmacological inhibitors to block ATP release in human aortic smooth...

Read the complete abstract on PubMed

Topics

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

Share to Aorta
Share to Autocrine Communication
Share to Becaplermin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Calponins

Share to Cell Dedifferentiation

Share to Myocytes, Smooth Muscle

Share to Myosin Heavy Chains

Share to Proto-Oncogene Proteins c-sis

Source

Open in PubMed Open full text

Identifiers

PMID: 38889566
DOI: 10.1016/j.atherosclerosis.2024.117613
PMCID: PMC11254552

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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

Basal ATP release signals through the P2Y2 receptor to maintain the differentiated phenotype of vascular smooth muscle cells.PMID 38889566Read ↗

PHB2 Maintains the Contractile Phenotype of VSMCs by Counteracting PKM2 Splicing.Semantic proximity Read ↗

Smooth muscle cell-driven vascular diseases and molecular mechanisms of VSMC plasticity.Semantic proximity Read ↗

The P2Y2 receptor mediates uptake of matrix-retained and aggregated low density lipoprotein in primary vascular smooth muscle cells.Semantic proximity Read ↗

Regulation of differentiation of vascular smooth muscle cellsSemantic proximity Read ↗

Dual role of PKA in phenotypic modulation of vascular smooth muscle cells by extracellular ATP.Semantic proximity Read ↗

Inhibition of vascular intimal hyperplasia by the myokine Musclin: the role of NPR3/raptor/mTORC1-mediated glycolysis and phenotypic switching of VSMCs.Semantic proximity Read ↗

Phenotypic Switching of Vascular Smooth Muscle Cells in Duchenne Muscular DystrophySemantic proximity Read ↗

Derivation and maturation of synthetic and contractile vascular smooth muscle cells from human pluripotent stem cellsSemantic proximity Read ↗

Hypoxia-induced miR-182-5p regulates vascular smooth muscle cell phenotypic switch by targeting RGS5.Semantic proximity Read ↗

Smooth muscle 22 alpha maintains the differentiated phenotype of vascular smooth muscle cells by inducing filamentous actin bundling.Semantic proximity Read ↗

Vascular smooth muscle cell phenotype is defined by Ca2+-dependent transcription factors.Semantic proximity Read ↗

Mitochondrial Protein Poldip2 (Polymerase Delta Interacting Protein 2) Controls Vascular Smooth Muscle Differentiated Phenotype by O-Linked GlcNAc (N-Acetylglucosamine) Transferase-Dependent Inhibition of a Ubiquitin Proteasome System.Semantic proximity Read ↗

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