ArticleBlood cells, molecules & diseases2015
Haptoglobin attenuates hemoglobin-induced heme oxygenase-1 in renal proximal tubule cells and kidneys of a mouse model of sickle cell disease.
Article in Blood cells, molecules & diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03111589 (Monocytic Expression of Heme Oxidase-1), which is not on this map. Cited by 31 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.
Monocytic Expression of Heme Oxidase-1 (HO-1) in Sickle Cell Patients and Correlation With the Humoral Immune Response to Vaccine and With Allo-immunization
Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
- Trial
- New orphan disease therapies from the proteome of industrial plasma processing waste- a treatment for aceruloplasminemia.Communications biology · 2024Article
- The clinical relevance of heme detoxification by the macrophage heme oxygenase system.Frontiers in immunology · 2024Review
- Article
- Cell-Free Hemoglobin in Acute Kidney Injury after Lung Transplantation and Experimental Renal Ischemia/Reperfusion.International journal of molecular sciences · 2022Article
- Different Acute Kidney Injury Patterns after Renal Ischemia Reperfusion Injury and Extracorporeal Membrane Oxygenation in Mice.International journal of molecular sciences · 2022Article
- Novel Insights into Alcoholic Liver Disease: Iron Overload, Iron Sensing and Hemolysis.Journal of translational internal medicine · 2022Article
- Relation between haptoglobin polymorphism and oxidative stress status, lipid profile, and cardiovascular risk in sickle cell anemia patients.Health science reports · 2022Article
- Haptoglobin treatment contributes to regulating nitric oxide signal and reduces oxidative stress in the penis: A preventive treatment for priapism in sickle cell disease.Frontiers in physiology · 2022Article
- Critical Role of Hemopexin Mediated Cytoprotection in the Pathophysiology of Sickle Cell Disease.International journal of molecular sciences · 2021Review
- Haptoglobin Gene Polymorphism among Sickle Cell Patients in West Cameroon: Hematological and Clinical Implications.Advances in hematology · 2021Article
- Exacerbation of Neonatal Hemolysis and Impaired Renal Iron Handling in Heme Oxygenase 1-Deficient Mice.International journal of molecular sciences · 2020Article
- Resuscitation From Hemorrhagic Shock With Fresh and Stored Blood and Polymerized Hemoglobin.Shock (Augusta, Ga.) · 2020Article
- Haptoglobin Gene Polymorphism in Patients with Sickle Cell Anemia: Findings from a Nigerian Cohort Study.The application of clinical genetics · 2020Article
- Cell-free hemoglobin augments acute kidney injury during experimental sepsis.American journal of physiology. Renal physiology · 2019Article
- Role of the kidneys in the redistribution of heme-derived iron during neonatal hemolysis in mice.Scientific reports · 2019Article
- Temporal and age-dependent effects of haptoglobin deletion on intracerebral hemorrhage-induced brain damage and neurobehavioral outcomes.Experimental neurology · 2019Article
- Oxidative pathways in the sickle cell and beyond.Blood cells, molecules & diseases · 2018Review
- Haptoglobin and hemopexin inhibit vaso-occlusion and inflammation in murine sickle cell disease: Role of heme oxygenase-1 induction.PloS one · 2018Article
- Dimethyl fumarate increases fetal hemoglobin, provides heme detoxification, and corrects anemia in sickle cell disease.JCI insight · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Sickle cell disease (SCD), a hereditary hemolytic disorder is characterized by chronic hemolysis, oxidative stress, vaso-occlusion and end-organ damage. Hemolysis releases toxic cell-free hemoglobin (Hb) into circulation. Under physiologic conditions, plasma Hb binds to haptoglobin (Hp) and forms Hb-Hp dimers. The dimers bind to CD163 receptors on macrophages for further internalization and degradation. However, in SCD patients plasma Hp is depleted and free Hb is cleared primarily by proximal tubules of kidneys. Excess free Hb in plasma predisposes patients to renal damage. We hypothesized that administration of exogenous Hp reduces Hb-mediated renal damage. To test this hypothesis, human renal proximal tubular cells (HK-2) were exposed to HbA (50μM heme) for 24h. HbA increased the expression of heme oxygenase-1 (HO-1), an enzyme which degrades heme, reduces heme-mediated oxidative toxicity, and confers cytoprotection. Similarly, infusion of HbA (32μM heme/kg) induced HO-1 expression in kidneys of SCD mice. Immunohistochemistry confirmed the increased HO-1 expression in the proximal tubules of the kidney. Exogenous Hp attenuated the HbA-induced HO-1 expression in vitro and in SCD mice. Our results suggest that Hb-mediated oxidative toxicity may contribute to renal damage in SCD and that Hp treatment reduces heme/iron toxicity in the kidneys following hemolysis.
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