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

PERK Is Dispensable for Smooth Muscle Cell Phenotype Switching in Atherosclerosis.

Arteriosclerosis, thrombosis, and vascular biology - 1 Jul 2026

Zhu Lucie Y, Xue Chenyi, Bashore Alexander C, Cui Jian, Yao Sicong, Sachs Nadja, Wettich Justus L, Coronel Johana, Garcia Enrique J, Khalid Shareef, Saleheen Danish, Li Mingyao, Maegdefessel Lars, Reilly Muredach P

Abstract excerpt

BACKGROUND: Smooth muscle cell (SMC)-derived cells form the bulk of cells in atherosclerotic lesions and modulate lesion stability and cardiovascular disease outcomes. Unfolded protein response (UPR) markers, thin fibrous caps, and inflammation correlate with human lesion instability and rupture. In mice, UPR drives macrophage and endothelial apoptosis and inflammation, but its impact on lesion stability through...

Read the complete abstract on PubMed

Topics

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

Share to Carotid Artery Diseases
Share to eIF-2 Kinase

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Hypercholesterolemia

Share to Muscle, Smooth, Vascular

Share to Myocytes, Smooth Muscle

Share to Plaque, Atherosclerotic

Share to Receptors, LDL

Share to Unfolded Protein Response

Source

Open in PubMed Open full text

Identifiers

PMID: 42131916
DOI: 10.1161/ATVBAHA.125.323869
PMCID: PMC13198416

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 16 Oct 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

PERK Is Dispensable for Smooth Muscle Cell Phenotype Switching in Atherosclerosis.PMID 42131916Read ↗

Stem Cell Pluripotency Genes Klf4 and Oct4 Regulate Complex SMC Phenotypic Changes Critical in Late-Stage Atherosclerotic Lesion Pathogenesis.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 ↗

LMO7 regulates smooth muscle cell cholesterol esterification to influence plaque stabilitySemantic proximity Read ↗

Atherosclerosis is a smooth muscle cell-driven tumor-like diseaseSemantic proximity Read ↗

Comprehensive Multimodal Profiling of Atherosclerosis Reveals Bhlhe40 as a Potential Regulator of Vascular Smooth Muscle Cell Phenotypic ModulationSemantic proximity Read ↗

From smooth to 'breaking bad': vascular smooth muscle cell phenotypic switching at the heart of plaque vulnerability.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 ↗

Single-Cell Genomics Reveals a Novel Cell State During Smooth Muscle Cell Phenotypic Switching and Potential Therapeutic Targets for Atherosclerosis in Mouse and Human.Semantic proximity Read ↗

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

Modulated smooth muscle cells accumulate late in human coronary atherosclerosis and are temporally and spatially linked to necrotic core formationSemantic proximity Read ↗

Transcriptomic, Specific Marker, and Pathway Analysis of Smooth Muscle Cell Foam Cells Relative to Macrophage Foam Cells in Human AtherosclerosisSemantic proximity Read ↗

Vascular Smooth Muscle–Specific NLRP3 Hyperactivation Drives Arterial Intimal Hyperplasia in MiceSemantic proximity Read ↗

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