ArticleJournal of clinical medicine2020
Mathematical Model Predicts Effective Strategies to Inhibit VEGF-eNOS Signaling.
Article in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Hypobaric Hypoxia Ameliorates Impaired Regeneration After Diabetic Skeletal Muscle Injury by Promoting HIF-1α Signaling.International journal of molecular sciences · 2026Article
- Multi-cellular network model predicts alterations in glomerular endothelial structure in diabetic kidney disease.PLoS computational biology · 2025Article
- The machinery of healthy vasodilatation: an overview.Pflugers Archiv : European journal of physiology · 2025Review
- A mechanistic computational model of HGF-VEGF-mediated endothelial cell proliferation and vascular permeability.iScience · 2025Article
- Logic-based modeling of inflammatory macrophage cross talk with glomerular endothelial cells in diabetic kidney disease.American journal of physiology. Renal physiology · 2025Article
- Case Report: Cadonilimab plus anlotinib with radiotherapy for lung adenocarcinoma with pancreatic metastasis in later-line therapy.Frontiers in immunology · 2025Article
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- Low-Intensity Pulsed Ultrasound: A Physical Stimulus with Immunomodulatory and Anti-inflammatory Potential.Annals of biomedical engineering · 2024Review
- The Contributions of Thrombospondin-1 to Epilepsy Formation.Neuroscience bulletin · 2024Review
- Cross-Domain Text Mining of Pathophysiological Processes Associated with Diabetic Kidney Disease.International journal of molecular sciences · 2024Article
- Endothelial cells signaling and patterning under hypoxia: a mechanistic integrative computational model including the Notch-Dll4 pathway.Frontiers in physiology · 2024Article
- Combining Multikinase Tyrosine Kinase Inhibitors Targeting the Vascular Endothelial Growth Factor and Cluster of Differentiation 47 Signaling Pathways Is Predicted to Increase the Efficacy of Antiangiogenic Combination Therapies.ACS pharmacology & translational science · 2023Article
- Systems biology of angiogenesis signaling: Computational models and omics.WIREs mechanisms of disease · 2022Review
- Mechanistic characterization of endothelial sprouting mediated by pro-angiogenic signaling.Microcirculation (New York, N.Y. : 1994) · 2022Article
- Article
- VEGFR-Mediated Cytotoxic Activity ofLife (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The endothelial nitric oxide synthase (eNOS) signaling pathway in endothelial cells has multiple physiological significances. It produces nitric oxide (NO), an important vasodilator, and enables a long-term proliferative response, contributing to angiogenesis. This signaling pathway is mediated by vascular endothelial growth factor (VEGF), a pro-angiogenic species that is often targeted to inhibit tumor angiogenesis. However, inhibiting VEGF-mediated eNOS signaling can lead to complications such as hypertension. Therefore, it is important to understand the dynamics of eNOS signaling in the context of angiogenesis inhibitors. Thrombospondin-1 (TSP1) is an important angiogenic inhibitor that, through interaction with its receptor CD47, has been shown to redundantly inhibit eNOS signaling. However, the exact mechanisms of TSP1's inhibitory effects on this pathway remain unclear. To address this knowledge gap, we established a molecular-detailed mechanistic model to describe VEGF-mediated eNOS signaling, and we used the model to identify the potential intracellular targets of TSP1. In addition, we applied the predictive model to investigate the effects of several approaches to selectively target eNOS signaling in cells experiencing high VEGF levels present in the tumor microenvironment. This work generates insights for pharmacologic targets and therapeutic strategies to inhibit tumor angiogenesis signaling while avoiding potential side effects in normal vasoregulation.
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