ArticleBiomolecules2024
Angiotensin II Induces Vascular Endothelial Dysfunction by Promoting Lipid Peroxidation-Mediated Ferroptosis via CD36.
Article in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
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Who cites it
20 citing papers in PubMed.
- Evaluation of Endothelial Dysfunction in Geriatric Patients with Non-Dialysis Chronic Kidney Disease.Journal of clinical medicine · 2026Article
- Cluster of Differentiation 36-Mediated Inflammation and Lipid Metabolism in Cardiovascular Diseases: From Mechanisms to Novel Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Senescent cells in systemic aging: SASP heterogeneity, immune escape, and endocrine modulation.Biogerontology · 2026Review
- Angiotensin II impairs the remyelination mediated by brain endothelial cell-derived exosomes.Acta neuropathologica communications · 2026Article
- Mitochondria-driven ferroptosis in intervertebral disc degeneration: A novel target in age-related spinal diseases (Review).Experimental and therapeutic medicine · 2026Review
- Antagonizing IL-17A Reduces Vascular Inflammation and Attenuates Oxidative Stress Formation but Does Not Significantly Improve Vascular Dysfunction Induced by One Week of Angiotensin II Treatment.Antioxidants (Basel, Switzerland) · 2026Article
- NAT10-Mediated ac4C-Modification Exacerbates Ferroptosis by Stabilizing HMOX1 in Deep Vein Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Review
- Occludin-mediated barrier dysfunction and its role in cardiovascular and cerebrovascular pathogenesis.Frontiers in cardiovascular medicine · 2026Review
- Molecular Interplay between hypertension and dyslipidemia in cardiovascular pathogenesis: toward precision-based therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Inhibition of S100A12 Attenuates LPS-induced Endothelial Barrier Dysfunction in HPMECs through the JAK2/STAT3 Signaling Pathway.Current molecular medicine · 2026Article
- Heart-Brain Axis Dysregulation in Depression: Mechanisms and Implications for Neuromodulation.Neuropsychiatric disease and treatment · 2026Review
- Does exercise modulate ferroptosis-related cardiovascular injury? Mechanistic evidence and translational boundaries.Frontiers in physiology · 2026Review
- Metabolic signatures and diagnostic models of ischemic stroke and its hypertensive subtype: a non-targeted metabolomics and machine learning.Frontiers in genetics · 2026Article
- Dietary Flavonoids as Cross-System Modulators of Hypertension and Intestinal Permeability.Molecules (Basel, Switzerland) · 2025Review
- Aspirin Eugenol Ester Alleviates Vascular Endothelial Ferroptosis by Enhancing Antioxidant Ability and Inhibiting the JNK/c-Jun/NCOA4/FTH Signaling Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- Beyond cardiac embolism and cryptogenic stroke: unveiling the mechanisms of cerebrovascular events in Chagas disease.Lancet regional health. Americas · 2025Review
- Potential novel diagnostic biomarkers of atrial fibrillation: four ferroptosis-related genes linking immune infiltration.European journal of medical research · 2025Article
- Mechanism-guided pharmacotherapy for cardiometabolic multimorbidity: from pathophysiology to phenotype-prioritized treatment.Frontiers in endocrinology · 2025Review
- Deciphering Oxidative Stress in Cardiovascular Disease Progression: A Blueprint for Mechanistic Understanding and Therapeutic Innovation.Antioxidants (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Angiotensin II (Ang II) is an effective vasoconstriction peptide, a major effector molecule of the renin-angiotensin-aldosterone system (RAAS) and one of the important causes of endothelial dysfunction. Ferroptosis is considered to be involved in the occurrence and development of cardiovascular diseases. This study is dedicated to exploring the role and mechanism of Ang II-induced ferroptosis in HUVECs and to finding molecular targets for vascular endothelial injury and dysfunction during the progression of hypertension. In this study, we found that with the increase in exposure concentration, the intracellular ROS content and apoptosis rate increased significantly, the NO release decreased significantly in the medium- and high-concentration groups and the ET-1 content in the high-concentration group increased significantly. The expression of ZO-1 protein was significantly decreased in the high-concentration group. The expression of p-eNOS, VE-cadherin and Occludin protein showed a dose-dependent downward trend, while the ICAM-1 protein showed an upward trend. Ang II caused lipid metabolism disorders in HUVECs, and the PL-PUFAs associated with ferroptosis were significantly increased. In addition, Ang II promoted a significant increase in intracellular free Fe
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Registered trials
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