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

Aquaporin 1 controls the functional phenotype of pulmonary smooth muscle cells in hypoxia-induced pulmonary hypertension.

Basic research in cardiology - 1 May 2017

Schuoler Claudio, Haider Thomas J, Leuenberger Caroline, Vogel Johannes, Ostergaard Louise, Kwapiszewska Grazyna, Kohler Malcolm, Gassmann Max, Huber Lars C, Brock Matthias

Abstract excerpt

Vascular remodelling in hypoxia-induced pulmonary hypertension (PH) is driven by excessive proliferation and migration of endothelial and smooth muscle cells. The expression of aquaporin 1 (AQP1), an integral membrane water channel protein involved in the control of these processes, is tightly regulated by oxygen levels. The role of AQP1 in the pathogenesis of PH, however, has not been directly addressed so far....

Read the complete abstract on PubMed

Topics

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

Share to Aquaporin 1
Share to Hypertension, Pulmonary

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hypoxia

Share to Muscle, Smooth, Vascular

Share to Myocytes, Smooth Muscle

Share to Pulmonary Artery

Share to Real-Time Polymerase Chain Reaction

Share to Vascular Remodeling

Source

Identifiers

PMID: 28409279
DOI: 10.1007/s00395-017-0620-7

Genes

AQP1

Provenance

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

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Aquaporin 1 controls the functional phenotype of pulmonary smooth muscle cells in hypoxia-induced pulmonary hypertension.PMID 28409279Read ↗

The aquaporin 1 C-terminal tail is required for migration and growth of pulmonary arterial myocytes.Semantic proximity Read ↗

Endothelial dysfunction in pulmonary arterial hypertension: an evolving landscape (2017 Grover Conference Series)Semantic proximity Read ↗

PTBP1 Targets ILK to Regulate the Hypoxia-Induced Phenotypic Transformation of Pulmonary Artery Smooth Muscle Cells.Semantic proximity Read ↗

Gene expression profiling of common signal transduction pathways affected by rBMSCs/F92A-Cav1 in the lungs of rat with pulmonary arterial hypertension.Semantic proximity Read ↗

Notch1 signalling regulates endothelial proliferation and apoptosis in pulmonary arterial hypertension.Semantic proximity Read ↗

Exosomes derived from hypoxic alveolar epithelial cells promote the phenotypic transformation of pulmonary artery smooth muscle cells via the Rap1 pathway.Semantic proximity Read ↗

Targeting Macrophage Crosstalk to PASMC by Blunting Inflammatory Phenotype Via SerpinB1 Protects Against Hypoxia-Induced Pulmonary Hypertension.Semantic proximity Read ↗

S1pr1 serves as a viable drug target against pulmonary fibrosis by increasing the integrity of the endothelial barrier of the lungSemantic proximity Read ↗

MiR-20a regulates the PRKG1 gene by targeting its coding region in pulmonary arterial smooth muscle cells.Semantic proximity Read ↗

Unraveling the role of HIF and epigenetic regulation in pulmonary arterial hypertension: implications for clinical research and its therapeutic approachSemantic proximity Read ↗

Overexpressed lncRNA AC068039.4 contributes to proliferation and cell cycle progression of pulmonary artery smooth muscle cells via sponging miR-26a-5p/TRPC6 in hypoxic pulmonary arterial hypertensionSemantic proximity Read ↗

The HIF2α-dependent upregulation of SETDB1 facilitates hypoxia-induced functional and phenotypical changes of pulmonary microvascular endothelial cells.Semantic proximity Read ↗

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