ArticleExperimental and therapeutic medicine2020
TMEM16A regulates the cell cycle of pulmonary artery smooth muscle cells in high-flow-induced pulmonary arterial hypertension rat model.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- ANO1 (TMEM16A) Genetic Variants, Promoter Methylation, and Chloride Dysregulation in Pulmonary Hypertension.Journal of cardiovascular development and disease · 2026Article
- TMEM16A channel signalling microdomains in the regulation of vascular function.The Journal of physiology · 2026Review
- The roles and functions of TMEM protein family members in cancers, cardiovascular and kidney diseases (Review).Biomedical reports · 2025Review
- Role of Sensory Nerves in Pulmonary Fibrosis.International journal of molecular sciences · 2024Review
- Editorial: Targeting pumps, channels and transporters for the treatments of vascular, cardiovascular and kidney diseases.Frontiers in pharmacology · 2023Article
- miR-155-5p regulates hypoxia-induced pulmonary artery smooth muscle cell function by targeting PYGL.Bioengineered · 2022Article
- Role of Ion Channel Remodeling in Endothelial Dysfunction Induced by Pulmonary Arterial Hypertension.Biomolecules · 2022Review
- Metabolic Reprogramming of the Right Ventricle and Pulmonary Arteries in a Flow-Associated Pulmonary Arterial Hypertension Rat Model.ACS omega · 2022Article
- Molecular mechanisms of activation and regulation of ANO1-Encoded CaChannels (Austin, Tex.) · 2021Review
- The diverse roles of TMEM16A CaJournal of advanced research · 2021Review
- The CaActa pharmaceutica Sinica. B · 2021Review
- Ginsenoside Rb1 Attenuates Triptolide-Induced Cytotoxicity in HL-7702 CellsFrontiers in pharmacology · 2021Article
- The mechanism of ions in pulmonary hypertension.Pulmonary circulationReview
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-flow-induced pulmonary arterial hypertension (PAH) has attained global notoriety, the mechanism of which remains elusive. The present study investigated the regulation of Anoctamin-1, also known as transmembrane member 16A (TMEM16A), in the cell cycle progression of pulmonary artery smooth muscle cells (PASMCs) from a PAH rat model induced by high pulmonary blood flow. A total of 30 Sprague-Dawley rats were randomly assigned into control, sham and shunt groups. A rat model of high pulmonary blood flow-induced PAH was established by surgery using abdominal aorta-inferior vena cava fistula. Right ventricular pressure, right ventricular hypertrophy index and pulmonary arteriole structural remodeling were assessed 11 weeks following operation. The cell cycle statuses of PASMCs was assessed via flow cytometry, whereas western blot analysis was performed to measure the expression of cyclin D1, CDK2, p27KIP and cyclin E in primary PASMCs isolated from rats. The expression of cyclin E and cyclin D1 was revealed to be increased in the shunt group compared with the control group, which was accompanied with an increased expression of TMEM16A in the shunt group. Changes in the ratio of PASMCs in the G
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