ArticleJournal of the American Heart Association2017
Monocrotaline Induces Endothelial Injury and Pulmonary Hypertension by Targeting the Extracellular Calcium-Sensing Receptor.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- Targeting Microglia-Neuron Crosstalk to Regulate Neuronal Excitability: Novel Translational Approaches for Chronic Pain Intervention.International journal of molecular sciences · 2026Review
- Pathophysiology of Pulmonary Arterial Hypertension: Focus on Vascular Endothelium as a Potential Therapeutic Target.International journal of molecular sciences · 2025Review
- Nobiletin alleviates hypoxia-induced pulmonary hypertension by inhibiting calcium-sensing receptor.Journal of natural medicines · 2025Article
- Cardioprotective effects of extracellular vesicles from hypoxia-preconditioned mesenchymal stromal cells in experimental pulmonary arterial hypertension.Stem cell research & therapy · 2025Article
- Feature-Tracking Method Can Estimate Right Ventricular Contractile Properties in Rats With Pulmonary Hypertension.Circulation reports · 2025Article
- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- Right ventricle remodelling: fromJournal of molecular and cellular cardiology plus · 2025Review
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- A novel dual fixation method for improving the reliable assessment of pulmonary vascular morphology in pulmonary hypertension rats.Respiratory research · 2025Article
- Hydrogen Inhalation Reduces Lung Inflammation and Blood Pressure in the Experimental Model of Pulmonary Hypertension in Rats.Biomedicines · 2023Article
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- The role of p53 in the alternation of vascular functions.Frontiers in pharmacology · 2022Review
- The roles of microRNAs played in lung diseases via regulating cell apoptosis.Molecular and cellular biochemistry · 2021Review
- Halofuginone, a promising drug for treatment of pulmonary hypertension.British journal of pharmacology · 2021Article
- Anti-Inflammatory Effect of Allicin Associated with Fibrosis in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2021Article
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- Endothelial-to-Mesenchymal Transition in Pulmonary Arterial Hypertension.Antioxidants & redox signaling · 2021Review
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- Calcium-sensing receptor in the development and treatment of pulmonary hypertension.Molecular biology reports · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMonocrotaline has been widely used to establish an animal model of pulmonary hypertension. The molecular target underlying monocrotaline-induced pulmonary artery endothelial injury and pulmonary hypertension remains unknown. The extracellular calcium-sensing receptor (CaSR) and particularly its extracellular domain hold the potential structural basis for monocrotaline to bind. This study aimed to reveal whether monocrotaline induces pulmonary hypertension by targeting the CaSR. METHODS AND
resultsNuclear magnetic resonance screening through WaterLOGSY (water ligand-observed gradient spectroscopy) and saturation transfer difference on protein preparation demonstrated the binding of monocrotaline to the CaSR. Immunocytochemical staining showed colocalization of monocrotaline with the CaSR in cultured pulmonary artery endothelial cells. Cellular thermal shift assay further verified the binding of monocrotaline to the CaSR in pulmonary arteries from monocrotaline-injected rats. Monocrotaline enhanced the assembly of CaSR, triggered the mobilization of calcium signaling, and damaged pulmonary artery endothelial cells in a CaSR-dependent manner. Finally, monocrotaline-induced pulmonary hypertension in rats was significantly attenuated or abolished by the inhibitor, the general or lung knockdown or knockout of CaSR.
conclusionsMonocrotaline aggregates on and activates the CaSR of pulmonary artery endothelial cells to trigger endothelial damage and, ultimately, induces pulmonary hypertension.
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