ArticleJournal of biochemical and molecular toxicology2021
Suppression of reactive oxygen species in endothelial cells by an antagonist of growth hormone-releasing hormone.
Article in Journal of biochemical and molecular toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- NEK kinases in cell cycle regulation, DNA damage response, and cancer progression.Tissue & cell · 2025Review
- GHRH and its analogues in central nervous system diseases.Reviews in endocrine & metabolic disorders · 2025Review
- Effects of GHRH and its analogues on the Vascular System.Reviews in endocrine & metabolic disorders · 2025Review
- Growth hormone - releasing hormone in the immune system.Reviews in endocrine & metabolic disorders · 2025Review
- Growth hormone-releasing hormone signaling and manifestations within the cardiovascular system.Reviews in endocrine & metabolic disorders · 2025Review
- Growth hormone - releasing hormone in the context of inflammation and redox biology.Frontiers in immunology · 2024Article
- Growth hormone-releasing hormone antagonists protect against hydrochloric acid-induced endothelial injury in vitro.Environmental toxicology and pharmacology · 2023Article
- Protective effects of GHRH antagonists against hydrogen peroxide-induced lung endothelial barrier disruption.Endocrine · 2023Article
- Growth hormone-releasing hormone antagonist MIA-602 inhibits inflammation induced by SARS-CoV-2 spike protein and bacterial lipopolysaccharide synergism in macrophages and human peripheral blood mononuclear cells.Frontiers in immunology · 2023Article
- Growth Hormone-Releasing Hormone in Endothelial Inflammation.Endocrinology · 2022Review
- Growth Hormone-Releasing Hormone Antagonist JV-1-36 Suppresses Reactive Oxygen Species Generation in A549 Lung Cancer Cells.Endocrines · 2022Article
- P53 mediates the protective effects of metformin in inflamed lung endothelial cells.International immunopharmacology · 2021Article
- Growth hormone suppression in endothelial dysfunction.Cell cycle (Georgetown, Tex.)Review
- Growth hormone-releasing hormone antagonists counteract hydrogen peroxide - induced paracellular hyperpermeability in endothelial cells.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research SocietyArticle
- Growth hormone in disease and treatment (Review).Medicine internationalReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Growth hormone-releasing hormone (GHRH) is a hypothalamic hormone, which regulates the secretion of growth hormone (GH) from the anterior pituitary gland. The effects of GHRH extend beyond the GH-insulin-like growth factor I axis, and that neuropeptide has been involved in the potentiation of several malignancies and other inflammatory disorders. The development of GHRH antagonists (GHRHAnt) delivers an exciting possibility to counteract the pathogenesis of the GHRH-related effects in human pathophysiology, especially when considered that GHRHAnt support endothelial barrier integrity. Those GHRHAnt-mediated effects are exerted at least in part due to the suppression of major inflammatory pathways, and the modulation of major cytoskeletal components. In the present study, we measured the production of reactive oxygen species (ROS) in bovine pulmonary artery endothelial cells, human cerebral microvascular endothelial cells, and human lung microvascular endothelial cells exposed to GHRH or a commercially available GHRHAnt. Our findings reveal the antioxidative effects of GHRHAnt in all three cell lines, which express GHRH receptors. The redox status of NIH/3T3 cells, which do not produce GHRH receptors, was not significantly affected by GHRH or GHRHAnt. Hence, the application of GHRHAnt in pathologies related to increased ROS production should be further investigated.
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Registered trials
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 OpenQuestion graph.