ArticleBritish journal of pharmacology2020
Transcriptomic analysis of pulmonary artery smooth muscle cells identifies new potential therapeutic targets for idiopathic pulmonary arterial hypertension.
Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- Deficiency of Smooth Muscle Adar1 Exacerbates Vascular Remodeling and Pulmonary Hypertension.Circulation research · 2026Article
- Role of lipid droplets in pulmonary arterial hypertension: focusing on pulmonary artery smooth muscle cell proliferation.Lipids in health and disease · 2025Review
- Hypoxanthine Promotes Pulmonary Vascular Remodeling and Adenosine Deaminase Is a Therapeutic Target for Pulmonary Hypertension.JACC. Basic to translational science · 2025Article
- Adventitial fibroblasts direct smooth muscle cell-state transition in pulmonary vascular disease.eLife · 2025Article
- Association of interferon regulator factor 1 upregulation with pulmonary arterial hypertension.Journal of thoracic disease · 2025Article
- Unraveling AURKB as a potential therapeutic target in pulmonary hypertension using integrated transcriptomic analysis and pre-clinical studies.Cell reports. Medicine · 2025Article
- CD44 as a novel therapeutic target in pulmonary arterial hypertension: Insights from multi-omics integration and molecular docking.PloS one · 2025Article
- Transcriptomic profiling highlights cell proliferation in the progression of experimental pulmonary hypertension in rats.Scientific reports · 2024Article
- Crocin's role in modulating MMP2/TIMP1 and mitigating hypoxia-induced pulmonary hypertension in mice.Scientific reports · 2024Article
- The COPD GWAS gene ADGRG6 instructs function and injury response in human iPSC-derived type II alveolar epithelial cells.American journal of human genetics · 2023Article
- Altered Smooth Muscle Cell Histone Acetylome by the SPHK2/S1P Axis Promotes Pulmonary Hypertension.Circulation research · 2023Article
- Purine synthesis suppression reduces the development and progression of pulmonary hypertension in rodent models.European heart journal · 2023Article
- Review
- An organ-on-chip model of pulmonary arterial hypertension identifies a BMPR2-SOX17-prostacyclin signalling axis.Communications biology · 2022Article
- HNRNPA2B1: RNA-Binding Protein That Orchestrates Smooth Muscle Cell Phenotype in Pulmonary Arterial Hypertension.Circulation · 2022Article
- Novel hub genes associated with pulmonary artery remodeling in pulmonary hypertension.Frontiers in cardiovascular medicine · 2022Article
- Review
- Disease-specific platelet signaling defects in idiopathic pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Molecular and Genetic Profiling for Precision Medicines in Pulmonary Arterial Hypertension.Cells · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
background and purposePulmonary arterial hypertension (PAH, type 1 pulmonary hypertension) has a 3-year survival of ~50% and is in need of new, effective therapies. In PAH, remodelling of the pulmonary artery (PA) increases pulmonary vascular resistance and can result in right heart dysfunction and failure. Genetic mutations can cause PAH but it can also be idiopathic (IPAH). Enhanced contractility and proliferation of PA smooth muscle cells (PASMCs) are key contributors to the pathophysiology of PAH, but the underlying mechanisms are not well understood. EXPERIMENTAL APPROACH: We utilized RNA-sequencing (RNA-seq) of IPAH and control patient-derived PASMCs as an unbiased approach to define differentially expressed (DE) genes that may identify new biology and potential therapeutic targets. KEY
resultsAnalysis of DE genes for shared gene pathways revealed increases in genes involved in cell proliferation and mitosis and decreases in a variety of gene sets, including response to cytokine signalling. ADGRG6/GPR126, an adhesion G protein-coupled receptor (GPCR), was increased in IPAH-PASMCs compared to control-PASMCs. Increased expression of this GPCR in control-PASMCs decreased their proliferation; siRNA knockdown of ADGRG6/GPR126 in IPAH-PASMCs tended to increase proliferation. CONCLUSION AND IMPLICATIONS: These data provide insights regarding the expression of current and experimental PAH drug targets, GPCRs and GPCR-related genes as potentially new therapeutic targets in PAH-PASMCs. Overall, the findings identify genes and pathways that may contribute to IPAH-PASMC function and suggest that ADGRG6/GPR126 is a novel therapeutic target for IPAH.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.