Therapeutic potential of haptoglobin in a murine model of sickle cell anemia
4 affiliations
- 1Laboratory for the Development of Biological Models, Multidisciplinary Center for Biological Research, University of Campinas (UNICAMP), Campinas, SP, Brazil
- 2Department of Pathology, Hemoglobinopathies Laboratory, School of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil
- 3Department of Pathology, Hematology Laboratory, Clinical Pathology Laboratory (LPC), University Hospital, School of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil
- 4Center for Hematology and Hemotherapy, National Institute of Science and Technology in Blood (INCTS), University of Campinas (UNICAMP), Campinas, SP, Brazil
Abstract
Chronic hemolytic anemia found in patients with sickle cell disease promotes an excess of free extracellular and intravascular hemoglobin, triggering a series of deleterious effects such as endothelial dysfunction, oxidative stress, and alterations in vascular tone, which lead to clinical complications. In this work, we evaluated the induced expression of haptoglobin in hepatocytes in vivo, the organism’s first line of defense to control the presence of free Hb in circulation, which becomes saturated in conditions of chronic hemolysis, such as sickle cell disease. Through gene therapy applied in a murine model of sickle cell anemia, we aimed to investigate whether this approach could interfere with disease progression and promote an improvement in the animals’ pathophysiological condition. The application of this treatment in the sickle cell anemia animal model resulted in significant therapeutic effects, including improvement of hematological parameters, reduction of the compensatory erythropoietic response, and attenuation of clinical signs such as splenomegaly. These results indicate that haptoglobin may act indirectly in the prevention of hemolysis, suggesting a new therapeutic approach.
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BibTeX
@article{santos2026therapeutic,
title = {{Therapeutic potential of haptoglobin in a murine model of sickle cell anemia}},
author = {Bianca Cristina dos Santos and Magnun Nueldo Nunes dos Santos and Gisele Audrei Pedroso and Beatriz Benedetti de Oliveira and Dulcinéia Martins de Albuquerque and Nathalia Rocha de Oliveira and Daniela Cagnoto Noronha and Fernando Ferreira Costa and Marcus Alexandre Finzi Corat},
journal = {PLOS One},
year = {2026},
month = sep,
doi = {10.1371/journal.pone.0357180},
url = {https://doi.org/10.1371/journal.pone.0357180},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Therapeutic potential of haptoglobin in a murine model of sickle cell anemia
AU - Bianca Cristina dos Santos
AU - Magnun Nueldo Nunes dos Santos
AU - Gisele Audrei Pedroso
AU - Beatriz Benedetti de Oliveira
AU - Dulcinéia Martins de Albuquerque
AU - Nathalia Rocha de Oliveira
AU - Daniela Cagnoto Noronha
AU - Fernando Ferreira Costa
AU - Marcus Alexandre Finzi Corat
PY - 2026
DA - 2026/09/18
JO - PLOS One
DO - 10.1371/journal.pone.0357180
UR - https://doi.org/10.1371/journal.pone.0357180
AB - Chronic hemolytic anemia found in patients with sickle cell disease promotes an excess of free extracellular and intravascular hemoglobin, triggering a series of deleterious effects such as endothelial dysfunction, oxidative stress, and alterations in vascular tone, which lead to clinical complications. In this work, we evaluated the induced expression of haptoglobin in hepatocytes in vivo, the organism’s first line of defense to control the presence of free Hb in circulation, which becomes saturated in conditions of chronic hemolysis, such as sickle cell disease. Through gene therapy applied in a murine model of sickle cell anemia, we aimed to investigate whether this approach could interfere with disease progression and promote an improvement in the animals’ pathophysiological condition. The application of this treatment in the sickle cell anemia animal model resulted in significant therapeutic effects, including improvement of hematological parameters, reduction of the compensatory erythropoietic response, and attenuation of clinical signs such as splenomegaly. These results indicate that haptoglobin may act indirectly in the prevention of hemolysis, suggesting a new therapeutic approach.
SN - 1932-6203
ER -