ArticleJournal of internal medicine2023
The red blood cell as a mediator of endothelial dysfunction in patients with familial hypercholesterolemia and dyslipidemia.
Article in Journal of internal medicine, 2023. 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.
- Loss of erythrocyte arginase-1 impairs vasorelaxation due to endothelial GSNOR overexpression and denitrosylation of G protein subunits.Redox biology · 2026Article
- Choice of lipid supplementation for in vitro erythroid cell culture impacts reticulocyte yield and characteristics.Scientific reports · 2026Article
- Redefining the concept of erythrocyte senescence: is eryptosis fundamentally different from erythrocyte senescence.GeroScience · 2025Review
- Maternal diabetes programs sexually dimorphic early-onset cardiovascular dysfunction in metabolically healthy offspring.Cell reports. Medicine · 2025Article
- Red Blood Cell Membrane Lipidomics: Potential Biomarkers Detecting Method for Plasma Volume Overload and Major Adverse Cardiovascular Events in Chronic Heart Failure Patients.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Erythrocyte-derived extracellular vesicles induce endothelial dysfunction through arginase-1 and oxidative stress in type 2 diabetes.The Journal of clinical investigation · 2025Article
- Endothelial Dysfunction: Redox Imbalance, NLRP3 Inflammasome, and Inflammatory Responses in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Platelet RNA-Seq Reveals Genes Associated with Carotid Intima-Media Thickness: A Cross-Sectional Study.TH open : companion journal to thrombosis and haemostasis · 2025Article
- Acute blood loss anemia aggravates endothelial dysfunction after acute myocardial infarction.Frontiers in cardiovascular medicine · 2025Article
- Development and validation of a predictive model for perioperative low-density lipoprotein as a risk factor for postoperative cerebral infarction in Moyamoya disease.Frontiers in neurology · 2025Article
- The Role of Red Blood Cells in Cholesterol Accumulation and Atherosclerotic Plaque Instability: A Perspective on Atherosclerosis.Current cardiology reviews · 2025Review
- New Insights into Endothelial Dysfunction in Cardiometabolic Diseases: Potential Mechanisms and Clinical Implications.International journal of molecular sciences · 2024Review
- iPSC-Derived Endothelial Cells Reveal LDLR Dysfunction and Dysregulated Gene Expression Profiles in Familial Hypercholesterolemia.International journal of molecular sciences · 2024Article
- Influence of Atherosclerotic Risk Factors on the Effectiveness of Therapeutic Ultrasound Cavitation for Flow Augmentation.Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography · 2024Article
- The red blood cell as a mediator of endothelial dysfunction in patients with familial hypercholesterolemia and dyslipidemia.Journal of internal medicine · 2023Article
- Unexplored Roles of Erythrocytes in Atherothrombotic Stroke.Neurology international · 2023Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPatients with familial hypercholesterolemia (FH) display high levels of low-density lipoprotein cholesterol (LDL-c), endothelial dysfunction, and increased risk of premature atherosclerosis. We have previously shown that red blood cells (RBCs) from patients with type 2 diabetes induce endothelial dysfunction through increased arginase 1 and reactive oxygen species (ROS).
objectiveTo test the hypothesis that RBCs from patients with FH (FH-RBCs) and elevated LDL-c induce endothelial dysfunction. METHODS AND
resultsFH-RBCs and LDL-c >5.0 mM induced endothelial dysfunction following 18-h incubation with isolated aortic rings from healthy rats compared to FH-RBCs and LDL-c <2.5 mM or RBCs from healthy subjects (H-RBCs). Inhibition of vascular but not RBC arginase attenuated the degree of endothelial dysfunction induced by FH-RBCs and LDL-c >5.0 mM. Furthermore, arginase 1 but not arginase 2 was elevated in the vasculature of aortic segments after incubation with FH-RBCs and LDL-c >5.0 mM. A superoxide scavenger, present throughout the 18-h incubation, attenuated the degree of endothelial dysfunction induced by FH-RBCs and LDL-c >5.0 mM. ROS production was elevated in these RBCs in comparison with H-RBCs. Scavenging of vascular ROS through various antioxidants also attenuated the degree of endothelial dysfunction induced by FH-RBCs and LDL-c >5.0 mM. This was corroborated by an increase in the lipid peroxidation product 4-hydroxynonenal. Lipidomic analysis of RBC lysates did not reveal any significant changes across the groups.
conclusionFH-RBCs induce endothelial dysfunction dependent on LDL-c levels via arginase 1 and ROS-dependent mechanisms.
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