ArticleBlood vessels, thrombosis & hemostasis2026
Sustained expression of hemopexin in an animal model of sickle cell anemia.
Article in Blood vessels, thrombosis & hemostasis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Augmenting hemopexin-mediated heme scavenging mitigates sepsis-induced acute kidney injury in humanized sickle cell mice.Blood vessels, thrombosis & hemostasis · 2026Article
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7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Sickle cell disease is a condition characterized by vaso-occlusive episodes and sustained hemolysis, leading to a chronic inflammatory state. Several studies have shown that the release of heme to the extracellular space due to hemolysis contributes to the inflammatory cascade observed in these patients. Hemopexin (HPX), the molecule responsible for removing excess heme from the circulation, is depleted in these patients. We have previously demonstrated that the IV infusion of an adeno-associated virus-based gene transfer vector was capable of inducing the transgenic expression of HPX in a dose-dependent manner in C57Bl6 mice. Here, we explored the effect of this vector in a mouse model of sickle cell anemia. Townes mice were transduced with 2 × 10
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