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

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

International journal of cardiology - 15 Oct 2018

Lin Hui, Ni Tingjuan, Zhang Jie, Meng Liping, Gao Feidan, Pan Sunlei, Luo Hangqi, Xu Fukang, Ru Guomei, Chi Jufang, Guo Hangyuan

Abstract excerpt

BACKGROUND: Phenotypic switching of vascular smooth muscle cells (VSMCs) plays a key role in atherosclerosis. We aimed to investigate whether Homocysteine-responsive endoplasmic reticulum protein (Herp) was involved in VSMC phenotypic switching and affected atheroprogression. METHODS: To assess the role of Herp in homocysteine (Hcy)-associated atherosclerosis, Herp-/- and LDLR-/- double knockout mice were...

Topics

Join the communities discussing this publication.

Atherosclerosis
Cell Proliferation
Gene Knockdown Techniques
Genes, Switch
Hyperhomocysteinemia

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Membrane Proteins

Muscle, Smooth, Vascular

Source

Identifiers

PMID: 30017525
DOI: 10.1016/j.ijcard.2018.07.043

Genes

LDLR
ATF6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

0

discussions

0

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Knockdown of Herp alleviates hyperhomocysteinemia mediated atherosclerosis through the inhibition of vascular smooth muscle cell phenotype switching.PMID 30017525Read ↗

New insights into phenotypic switching of VSMCs induced by hyperhomocysteinemia: Role of endothelin-1 signaling.Semantic proximity Read ↗

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

Cholesterol-Induced Phenotypic Modulation of Smooth Muscle Cells to Macrophage/Fibroblast-like Cells Is Driven by an Unfolded Protein Response.Semantic proximity Read ↗

An update on the phenotypic switching of vascular smooth muscle cells in the pathogenesis of atherosclerosis.Semantic proximity Read ↗

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

HRD1 reduction promotes cholesterol-induced vascular smooth muscle cell phenotypic change via endoplasmic reticulum stress.Semantic proximity Read ↗

Deficiency of protein inhibitor of activated STAT3 exacerbates atherosclerosis by modulating VSMC phenotypic switching.Semantic proximity Read ↗

Atherosclerotic plaque-derived extracellular vesicles mediate smooth muscle cell phenotypic switching and promote vascular remodeling : EVs promote VSMC phenotypic switching.Semantic proximity Read ↗

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

Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases.Semantic proximity Read ↗

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

Phenotypic switching of vascular smooth muscle cells in atherosclerosis, hypertension, and aortic dissection.Semantic proximity Read ↗

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