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

Protein deglycase DJ-1 deficiency induces phenotypic switching in vascular smooth muscle cells and exacerbates atherosclerotic plaque instability.

Journal of cellular and molecular medicine - 1 Mar 2021

Wang Zhao-Yang, Cheng Jie, Liu Bin, Xie Fei, Li Chang-Ling, Qiao Wen, Lu Qing-Hua, Wang Ying, Zhang Ming-Xiang

Abstract excerpt

Protein deglycase DJ-1 (DJ-1) is a multifunctional protein involved in various biological processes. However, it is unclear whether DJ-1 influences atherosclerosis development and plaque stability. Accordingly, we evaluated the influence of DJ-1 deletion on the progression of atherosclerosis and elucidate the underlying mechanisms. We examine the expression of DJ-1 in atherosclerotic plaques of human and mouse...

Read the complete abstract on PubMed

Topics

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

Share to Carotid Arteries
Share to Kruppel-Like Factor 4

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Kruppel-Like Transcription Factors

Share to Lipoproteins, LDL

Share to Muscle, Smooth, Vascular

Share to Myocytes, Smooth Muscle

Share to Plaque, Atherosclerotic

Share to Protein Deglycase DJ-1

Source

Open in PubMed Open full text

Identifiers

PMID: 33501750
DOI: 10.1111/jcmm.16311
PMCID: PMC7957272

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

Protein deglycase DJ-1 deficiency induces phenotypic switching in vascular smooth muscle cells and exacerbates atherosclerotic plaque instability.PMID 33501750Read ↗

Thrombospondin-1 deficiency accelerates atherosclerotic plaque maturation in ApoE-/- mice.Semantic proximity Read ↗

PDIA1 acts as master organizer of NOX1/NOX4 balance and phenotype response in vascular smooth muscle.Semantic proximity Read ↗

Proteomic Analysis of Aorta and Protective Effects of Grape Seed Procyanidin B2 in db/db Mice Reveal a Critical Role of Milk Fat Globule Epidermal Growth Factor-8 in Diabetic Arterial DamageSemantic proximity Read ↗

UFM1 suppresses VSMCs phenotypic switching and attenuates atherosclerosis by inhibiting AKT phosphorylation.Semantic proximity Read ↗

IGF-1 has plaque-stabilizing effects in atherosclerosis by altering vascular smooth muscle cell phenotype.Semantic proximity Read ↗

Syndecan-1 as a predictor of vulnerable atherosclerotic plaquesSemantic proximity Read ↗

ANGPTL4 stabilizes atherosclerotic plaques and modulates the phenotypic transition of vascular smooth muscle cells through KLF4 downregulation.Semantic proximity Read ↗

Sentrin-specific protease 3 (SENP3)-mediated Krüppel-like factor 4 (KLF4) deSUMOylation regulates vascular smooth muscle cell phenotypic switching in atherosclerosis.Semantic proximity Read ↗

DKK3 (Dickkopf 3) Alters Atherosclerotic Plaque Phenotype Involving Vascular Progenitor and Fibroblast Differentiation Into Smooth Muscle Cells.Semantic proximity Read ↗

A Novel Mouse Model of Atherosclerotic Plaque Instability for Drug Testing and Mechanistic/Therapeutic Discoveries Using Gene and MicroRNA Expression ProfilingSemantic proximity Read ↗

Loss of Down syndrome critical region-1 leads to cholesterol metabolic dysfunction that exaggerates hypercholesterolemia in ApoE-null background.Semantic proximity Read ↗

Mindin regulates vascular smooth muscle cell phenotype and prevents neointima formation.Semantic proximity Read ↗

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