ArticleInternational journal of molecular sciences2022
Metabolic Response in Endothelial Cells to Catecholamine Stimulation Associated with Increased Vascular Permeability.
Article in International journal of molecular sciences, 2022. 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, 19 citations in OpenAlex.
- Shock Induced Endotheliopathy and High Trauma Mortality-Fight-or-Flight Response Revisited.International journal of molecular sciences · 2026Review
- Microparticles at the crossroads of the gut-kidney axis: Mechanistic drivers and therapeutic horizons in hemodialysis.World journal of nephrology · 2026Review
- Venous Nanoflap Oscillations: Biomechanical Determinants and Hydrodynamic Consequences in the Deep Cerebral Venous System.International journal of molecular sciences · 2026Review
- Sympathetic Stress and Sleep Loss in Diabetic Retinopathy: Links to Retinal Blood-Flow Control.Biomedicines · 2026Review
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- The brain-skin connection: A narrative review of neuroendocrine and immune pathways.JAAD international · 2026Article
- Pro- and Anti-Inflammatory Responses and Clinical Outcomes in Critically Ill Patients With Endotheliopathy: A Cohort Study.Acta anaesthesiologica Scandinavica · 2025Article
- Autonomic dysfunction after stroke: an overview of recent clinical evidence and perspectives on therapeutic management.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025Review
- Catecholamines in sepsis: pharmacological insights and clinical applications-a narrative review.Journal of anesthesia, analgesia and critical care · 2025Review
- Loneliness associates with endothelial dysfunction in a community-based cohort: a pilot study and translational approach.NPJ cardiovascular health · 2025Article
- Coadministration of PEGylated apohemoglobin and haptoglobin can limit vascular dysfunction in the microcirculation and prevent acute inflammation.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Article
- Blunted brachial blood flow velocity response to acute mental stress in PTSD females.Physiological reports · 2024Article
- Blood failure: traumatic hemorrhage and the interconnections between oxygen debt, endotheliopathy, and coagulopathy.Clinical and experimental emergency medicine · 2024Article
- Endothelial Cell Dysfunction and Increased Cardiovascular Risk in Patients With Chronic Kidney Disease.Circulation research · 2023Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Disruption to endothelial cell homeostasis results in an extensive variety of human pathologies that are particularly relevant to major trauma. Circulating catecholamines, such as adrenaline and noradrenaline, activate endothelial adrenergic receptors triggering a potent response in endothelial function. The regulation of the endothelial cell metabolism is distinct and profoundly important to endothelium homeostasis. However, a precise catalogue of the metabolic alterations caused by sustained high catecholamine levels that results in endothelial dysfunction is still underexplored. Here, we uncover a set of up to 46 metabolites that exhibit a dose-response relationship to adrenaline-noradrenaline equimolar treatment. The identified metabolites align with the glutathione-ascorbate cycle and the nitric oxide biosynthesis pathway. Certain key metabolites, such as arginine and reduced glutathione, displayed a differential response to treatment in early (4 h) compared to late (24 h) stages of sustained stimulation, indicative of homeostatic metabolic feedback loops. Furthermore, we quantified an increase in the glucose consumption and aerobic respiration in endothelial cells upon catecholamine stimulation. Our results indicate that oxidative stress and nitric oxide metabolic pathways are downstream consequences of endothelial cell stimulation with sustained high levels of catecholamines. A precise understanding of the metabolic response in endothelial cells to pathological levels of catecholamines will facilitate the identification of more efficient clinical interventions in trauma patients.
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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.