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

Angiopoietin-like 4 facilitates human aortic smooth muscle cell phenotype switch and dysfunctions through the PI3K/Akt signaling in aortic dissection.

Advances in medical sciences - 1 Sept 2024

He Wei, Zheng Quan, Zou Tingfang, Yan Wei, Gao Xue, Wang Chunle, Xiong Yaoyao

Abstract excerpt

PURPOSE: Vascular smooth muscle cell (VSMC) phenotype switch and dysfunctions have been reported to participate in aortic dissection (AD) progression. This study was aimed to investigate the role of angiopoietin-like 4 (ANGPTL4) in regulating VSMCs phenotype switch. MATERIALS AND METHODS: Key genes were analyzed in AD using public datasets, and it was found that the central differential gene ANGPTL4 was...

Read the complete abstract on PubMed

Topics

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

Share to Aorta
Share to Aortic Dissection

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Movement

Share to Cells, Cultured

Share to Muscle, Smooth, Vascular

Share to Myocytes, Smooth Muscle

Share to Phosphatidylinositol 3-Kinases

Share to Proto-Oncogene Proteins c-akt

Source

Identifiers

PMID: 39326736
DOI: 10.1016/j.advms.2024.09.006

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Angiopoietin-like 4 facilitates human aortic smooth muscle cell phenotype switch and dysfunctions through the PI3K/Akt signaling in aortic dissection.PMID 39326736Read ↗

LINC01278 Sponges miR-500b-5p to Regulate the Expression of ACTG2 to Control Phenotypic Switching in Human Vascular Smooth Muscle Cells During Aortic Dissection.Semantic proximity Read ↗

Integrin α9 is involved in the pathopoiesis of acute aortic dissection via mediating phenotype switch of vascular smooth muscle cell.Semantic proximity Read ↗

Long non-coding RNA HIF1A-AS2 modulates the proliferation, migration, and phenotypic switch of aortic smooth muscle cells in aortic dissection via sponging microRNA-33b.Semantic proximity Read ↗

Involvement of Oct4 in the pathogenesis of thoracic aortic dissection via inducing the dedifferentiated phenotype of human aortic smooth muscle cells by directly upregulating KLF5.Semantic proximity Read ↗

Circ_TGFBR2 Inhibits Vascular Smooth Muscle Cells Phenotypic Switch and Suppresses Aortic Dissection Progression by Sponging miR-29aSemantic proximity Read ↗

Progression of Thoracic Aortic Dissection Is Aggravated by the hsa_circ_0007386/miR-1271-5P/IGF1R/AKT Axis via Induction of Arterial Smooth Muscle Cell ApoptosisSemantic proximity Read ↗

How vascular smooth muscle cell phenotype switching contributes to vascular disease.Semantic proximity Read ↗

Dysregulation of interaction between LOXhigh fibroblast and smooth muscle cells contributes to the pathogenesis of aortic dissectionSemantic proximity Read ↗

Anxa1 in smooth muscle cells protects against acute aortic dissection.Semantic proximity Read ↗

sGC agonist BAY1021189 promotes thoracic aortic dissection formation by accelerating vascular smooth muscle cell phenotype switch.Semantic proximity Read ↗

Unveiling cellular and molecular aspects of ascending thoracic aortic aneurysms and dissections.Semantic proximity Read ↗

Single‐Cell RNA ‐Seq Reveals Injuries in Aortic Dissection and Identifies PDGF Signalling Pathway as a Potential Therapeutic TargetSemantic proximity Read ↗

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