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

Soluble epoxide hydrolase inhibitor, TPPU, attenuates progression of atherosclerotic lesions and vascular smooth muscle cell phenotypic switching.

Vascular pharmacology - 1 Aug 2022

Kim So Ah, Lee Ae Sin, Lee Han Bit, Hur Haeng Jeon, Lee Sang Hee, Sung Mi Jeong

Abstract excerpt

Atherosclerosis manifests as a chronic inflammation resulting from multiple interactions between circulating factors and various cell types in blood vessel walls. Growing evidence shows that phenotypic switching and proliferation of vascular smooth muscle cells (VSMCs) plays an important role in the progression of atherosclerosis. Soluble epoxide hydrolase (sEH)/epoxyeicosatrienoic acids are mediated by vascular...

Read the complete abstract on PubMed

Topics

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

Share to Apolipoproteins E
Share to Atherosclerosis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Epoxide Hydrolases

Share to Homocysteine

Share to Muscle, Smooth, Vascular

Share to Myocytes, Smooth Muscle

Source

Identifiers

PMID: 35752378
DOI: 10.1016/j.vph.2022.107086

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

Soluble epoxide hydrolase inhibitor, TPPU, attenuates progression of atherosclerotic lesions and vascular smooth muscle cell phenotypic switching.PMID 35752378Read ↗

Piperlonguminine attenuates atherosclerosis in mice via phenotype switching inhibition of vascular smooth muscle cells.Semantic proximity Read ↗

Soluble epoxide hydrolase is involved in the development of atherosclerosis and arterial neointima formation by regulating smooth muscle cell migration.Semantic proximity Read ↗

Knockdown of Herp alleviates hyperhomocysteinemia mediated atherosclerosis through the inhibition of vascular smooth muscle cell phenotype switching.Semantic proximity Read ↗

Hcy regulates SIRT1-STAT3 phosphorylation by upregulating WWP2 expression and induce VSMCs proliferation, migration, and phenotypic switch.Semantic proximity Read ↗

Artesunate inhibits macrophage-like phenotype switching of vascular smooth muscle cells and attenuates vascular inflammatory injury in atherosclerosis via NLRP3.Semantic proximity Read ↗

Trimethylamine-N-oxide affects cell type-specific pathways and networks in mouse aorta to promote atherosclerotic plaque vulnerabilitySemantic proximity Read ↗

Inactivation of semicarbazide-sensitive amine oxidase induces the phenotypic switch of smooth muscle cells and aggravates the development of atherosclerotic lesions.Semantic proximity Read ↗

Melatonin Ameliorates Atherosclerotic Plaque Vulnerability by Regulating PPARδ-Associated Smooth Muscle Cell Phenotypic Switching.Semantic proximity Read ↗

Berberine Inhibits Abdominal Aortic Aneurysm Formation and Vascular Smooth Muscle Cell Phenotypic Switching by Regulating the Nrf2 Pathway.Semantic proximity Read ↗

Activation of M3AChR (Type 3 Muscarinic Acetylcholine Receptor) and Nrf2 (Nuclear Factor Erythroid 2-Related Factor 2) Signaling by Choline Alleviates Vascular Smooth Muscle Cell Phenotypic Switching and Vascular Remodeling.Semantic proximity Read ↗

Role of Diverse Smooth Muscle Cell Phenotypic Transitions in Atherosclerosis Development and Late-Stage Pathogenesis.Semantic proximity Read ↗

Epidrugs in the clinical management of atherosclerosis: Mechanisms, challenges and promisesSemantic proximity Read ↗

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