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

ETAR silencing ameliorated neurovascular injury after SAH in rats through ERK/KLF4-mediated phenotypic transformation of smooth muscle cells.

Experimental neurology - 1 Mar 2021

Zhang Zhaosi, Chen Hong, Liu Liu, Zhao Guosheng, He Junchi, Liu Han, Zhou Chao, Liu Xiaoshuang, Sun Xiaochuan, Guo Zongduo

Abstract excerpt

Subarachnoid haemorrhage (SAH) is a devastating cerebrovascular disease which has a high morbidity and mortality. The phenotypic transformation of smooth muscle cells (SMCs) lead to neurovascular injury after SAH. However, the underlying mechanism remains unclear. In the present study, we aimed to investigate the potential role of ET-1/ETAR on the phenotypic transformation of SMCs after SAH. The models of SAH...

Read the complete abstract on PubMed

Topics

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

Share to Cerebrovascular Circulation
Share to Endothelin-1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Kruppel-Like Factor 4

Share to Kruppel-Like Transcription Factors

Share to Myocytes, Smooth Muscle

Share to Receptor, Endothelin A

Share to Receptors, Endothelin

Share to Subarachnoid Hemorrhage

Source

Identifiers

PMID: 33417892
DOI: 10.1016/j.expneurol.2021.113596

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

ETAR silencing ameliorated neurovascular injury after SAH in rats through ERK/KLF4-mediated phenotypic transformation of smooth muscle cells.PMID 33417892Read ↗

Phenotypic transformation of smooth muscle in vasospasm after aneurysmal subarachnoid hemorrhage.Semantic proximity Read ↗

PDGFR-β modulates vascular smooth muscle cell phenotype via IRF-9/SIRT-1/NF-κB pathway in subarachnoid hemorrhage rats.Semantic proximity Read ↗

Smooth muscle cell phenotypic switching in stroke.Semantic proximity Read ↗

Hemoglobin induced NO/cGMP suppression Deteriorate Microcirculation via Pericyte Phenotype Transformation after Subarachnoid Hemorrhage in Rats.Semantic proximity Read ↗

Vascular smooth muscle cells in intracranial aneurysms.Semantic proximity Read ↗

Zinc finger GATA-like protein 1 regulates apoptosis and phenotypic transformation via protein kinase B pathway in human vascular smooth muscle cells.Semantic proximity Read ↗

Regulatory mechanism of human vascular smooth muscle cell phenotypic transformation induced by NELIN.Semantic proximity Read ↗

PPARβ/δ, a Novel Regulator for Vascular Smooth Muscle Cells Phenotypic Modulation and Vascular Remodeling after Subarachnoid Hemorrhage in Rats.Semantic proximity Read ↗

Atorvastatin regulates vascular smooth muscle cell phenotypic transformation by epigenetically modulating contractile proteins and mediating Akt/FOXO4 axis.Semantic proximity Read ↗

Phenotypic modulation of smooth muscle cells and vascular remodeling in intraparenchymal small cerebral arteries after canine experimental subarachnoid hemorrhage.Semantic proximity Read ↗

Abnormalities of endothelial function in the pathogenesis of stroke: the importance of endothelin.Semantic proximity Read ↗

Liraglutide blocks the proliferation, migration and phenotypic switching of Homocysteine (Hcy)-induced vascular smooth muscle cells (VSMCs) by suppressing proprotein convertase subtilisin kexin9 (PCSK9)/ low-density lipoprotein receptor (LDLR).Semantic proximity Read ↗

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