ReviewFrontiers in physiology2014
Red blood cell, hemoglobin and heme in the progression of atherosclerosis.
Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
59 citing papers in PubMed, 118 citations in OpenAlex.
- Glucose-6-Phosphate Dehydrogenase Deficiency Reprograms Macrophage Metabolism in Hyperlipidemia.Blood red cells & iron · 2026Article
- Spectral characterization of advanced glycation end products in human hemoglobin, serum albumin, and erythrocytes.Biomedical optics express · 2026Article
- Effects of prosthetic heart valve-associated subclinical intravascular hemolysis on endothelium and cardiovascular system: a retrospective cohort study.Heart and vessels · 2026Article
- The Role of Red Blood Cells in Cholesterol Accumulation and Atherosclerotic Plaque Instability: A Perspective on Atherosclerosis.Current cardiology reviews · 2025Review
- Hemin-induced platelet activation is regulated by the ACKR3 chemokine surface receptor and has implications for passivation of vulnerable atherosclerotic plaques.The FEBS journal · 2024Article
- Interaction of carbonic anhydrase I released from red blood cells with human plasma in vitro.Metallomics : integrated biometal science · 2024Article
- Sonodynamic therapy for the treatment of atherosclerosis.Journal of pharmaceutical analysis · 2024Review
- Molecular Pathways of Vulnerable Carotid Plaques at Risk of Ischemic Stroke: A Narrative Review.International journal of molecular sciences · 2024Review
- The accumulation of erythrocytes quantified and visualized by Glycophorin C in carotid atherosclerotic plaque reflects intraplaque hemorrhage and pre-procedural neurological symptoms.Scientific reports · 2023Article
- Pharmacological Prevention of Ectopic Erythrophagocytosis by Cilostazol Mitigates Ferroptosis in NASH.International journal of molecular sciences · 2023Article
- Heme: The Lord of the Iron Ring.Antioxidants (Basel, Switzerland) · 2023Review
- Blind spectral unmixing for characterization of plaque composition based on multispectral photoacoustic imaging.Scientific reports · 2023Article
- Fundamental Pathobiology of Coronary Atherosclerosis and Clinical Implications for Chronic Ischemic Heart Disease Management-The Plaque Hypothesis: A Narrative Review.JAMA cardiology · 2023Review
- Prediction models for major adverse cardiovascular events following ST-segment elevation myocardial infarction and subgroup-specific performance.Frontiers in cardiovascular medicine · 2023Article
- Potential intervention target of atherosclerosis: Ferroptosis (Review).Molecular medicine reports · 2022Review
- Modulators of Nitric Oxide-Dependent Osteoinductive Activity of Human Red Blood Cells.TH open : companion journal to thrombosis and haemostasis · 2022Article
- Differential Gene Expression and Immune Cell Infiltration in Carotid Intraplaque Hemorrhage Identified Using Integrated Bioinformatics Analysis.Frontiers in cardiovascular medicine · 2022Article
- Sex-Specific Differences of Adenosine Triphosphate Levels in Red Blood Cells Isolated From ApoE/LDLR Double-Deficient Mice.Frontiers in physiology · 2022Article
- Hemoglobin induces inflammation through NF-kB signaling pathway and causes cell oxidative damage in grass carp (Frontiers in immunology · 2022Article
- Development of hydrogen sulfide donors for anti-atherosclerosis therapeutics research: Challenges and future priorities.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For decades plaque neovascularization was considered as an innocent feature of advanced atherosclerotic lesions, but nowadays growing evidence suggest that this process triggers plaque progression and vulnerability. Neovascularization is induced mostly by hypoxia, but the involvement of oxidative stress is also established. Because of inappropriate angiogenesis, neovessels are leaky and prone to rupture, leading to the extravasation of red blood cells (RBCs) within the plaque. RBCs, in the highly oxidative environment of the atherosclerotic lesions, tend to lyse quickly. Both RBC membrane and the released hemoglobin (Hb) possess atherogenic activities. Cholesterol content of RBC membrane contributes to lipid deposition and lipid core expansion upon intraplaque hemorrhage. Cell-free Hb is prone to oxidation, and the oxidation products possess pro-oxidant and pro-inflammatory activities. Defense and adaptation mechanisms evolved to cope with the deleterious effects of cell free Hb and heme. These rely on plasma proteins haptoglobin (Hp) and hemopexin (Hx) with the ability to scavenge and eliminate free Hb and heme form the circulation. The protective strategy is completed with the cellular heme oxygenase-1/ferritin system that becomes activated when Hp and Hx fail to control free Hb and heme-mediated stress. These protective molecules have pharmacological potential in diverse pathologies including atherosclerosis.
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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.