ArticleCell proliferation2018
The transient receptor potential vanilloid-3 regulates hypoxia-mediated pulmonary artery smooth muscle cells proliferation via PI3K/AKT signaling pathway.
Article in Cell proliferation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
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- Bellidifolin Improves Pulmonary Artery Smooth Muscle Cells Proliferation by Targeting the IGFBP5-Mediated PI3K-AKT-mTOR Pathway and Dilates the Pulmonary Artery.Biomolecules · 2026Article
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
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- Lung microbiome: new insights into the pathogenesis of respiratory diseases.Signal transduction and targeted therapy · 2024Review
- Challenges and Future Trends in Atopic Dermatitis.International journal of molecular sciences · 2023Review
- Gut microbiota crosstalk mechanisms are key in pulmonary hypertension: The involvement of melatonin is instrumental too.Pulmonary circulation · 2023Review
- Novel Insights into the Role of Keratinocytes-Expressed TRPV3 in the Skin.Biomolecules · 2023Review
- The nuclear transportation of PD-L1 and the function in tumor immunity and progression.Cancer immunology, immunotherapy : CII · 2022Review
- MicroRNA miR-627-5p restrains pulmonary artery smooth muscle cell dysfunction by targeting MAP 2 K4 and PI3K/AKT signaling.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2022Article
- CaInternational journal of molecular sciences · 2022Review
- Potential mechanisms of Qili Qiangxin capsule to prevent pulmonary arterial hypertension based on network pharmacology analysis in a rat model.Annals of translational medicine · 2022Article
- The zinc transporter ZIP12 regulates monocrotaline-induced proliferation and migration of pulmonary arterial smooth muscle cells via the AKT/ERK signaling pathways.BMC pulmonary medicine · 2022Article
- Potential of the TRPM7 channel as a novel therapeutic target for pulmonary arterial hypertension.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2022Review
- Bioinformatic Exploration of Hub Genes and Potential Therapeutic Drugs for Endothelial Dysfunction in Hypoxic Pulmonary Hypertension.Computational and mathematical methods in medicine · 2022Article
- Construction of a diagnostic signature and immune landscape of pulmonary arterial hypertension.Frontiers in cardiovascular medicine · 2022Article
- Mechanism of Hypoxia-Mediated Smooth Muscle Cell Proliferation Leading to Vascular Remodeling.BioMed research international · 2022Review
- Cellular mechanosignaling in pulmonary arterial hypertension.Biophysical reviews · 2021Review
- TRIM32 inhibits the proliferation and migration of pulmonary artery smooth muscle cells through the inactivation of PI3K/Akt pathway in pulmonary arterial hypertension.Journal of bioenergetics and biomembranes · 2021Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectvesTransient receptor potential vanilloid 3 (TRPV3) is a member of the TRP channels family of Ca MATERIALS AND
methodsThe expression of TRPV3 was evaluated in patients with pulmonary arterial hypertension (PAH) and hypoxic rats, using hematoxylin and eosin (H&E) and immunohistochemistry. In vitro, MTT assay, flow cytometry, Western blotting and immunofluorescence were performed to investigate the effects of TRPV3 on proliferation of PASMCs.
resultsWe found that, in vivo, the expression of TRPV3 was increased in patients with PAH and hypoxic rats. Right ventricular hypertrophy measurements and pulmonary pathomorphology data show that the ratio of the heart weight/tibia length (HW/TL), the right ventricle/left ventricle plus septum (RV/LV+S) and the medial width of the pulmonary artery were increased in chronic hypoxic rats. Moreover, the expression of proliferating cell nuclear antigen (PCNA), Cyclin D, Cyclin E and Cyclin A, phospho-CaMKII (p-CaMKII) were induced by hypoxia. In vitro, we revealed that hypoxia promoted PASMCs viability, increased the expression of PCNA, Cyclin D, Cyclin E, Cyclin A p-CaMKII, made more cells from G
conclusionsThese findings suggest that TRPV3 is involved in hypoxia-induced pulmonary vascular remodeling and promotes proliferation of PASMCs and the effect is, at least in part, mediated via the PI3K/AKT pathway.
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