ArticleEMBO reports2026
Liver sinusoidal endothelial cells constitute a major route for hemoglobin clearance.
Article in EMBO reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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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
4 citing papers in PubMed.
- Liver sinusoidal endothelial cells in liver diseases and hepatocellular carcinoma: molecular mechanisms, physiology, and therapies.Molecular biomedicine · 2026Review
- The Queen and the Dark Twin: Heme, Protoporphyrin IX, and State Transitions in Liver Metabolism.Molecules (Basel, Switzerland) · 2026Review
- Review
- Transmission Electron Microscopy Corneal Ultrastructure Study in Hematocornea of Corneal Transplant Graft.Diagnostics (Basel, Switzerland) · 2026Article
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
Mild rupture of aged erythrocytes occurs in the spleen, resulting in hemoglobin (Hb) release, whereas pathological hemolysis characterizes several diseases. Hb detoxification is attributed to macrophages, but other routes of Hb clearance remain elusive. Here, we uncover that Hb uptake is chiefly executed by liver sinusoidal endothelial cells (LSECs) via macropinocytosis. Consistently, LSECs display proteomic signatures indicative of heme catabolism, ferritin iron storage, antioxidant defense, and macropinocytic capacity, alongside high iron content and expression of the iron exporter ferroportin. Erythrocyte/Hb transfusion assays demonstrate that splenic macrophages excel in erythrophagocytosis, while LSECs and Kupffer cells scavenge the spleen-borne hemolysis products Hb and erythrocyte membranes, respectively. High Hb doses result in transient hepatic iron retention, LSEC-specific induction of heme-catabolizing Hmox1, along with the iron-sensing Bmp6-hepcidin axis culminating in hypoferremia. Transcriptional induction of Bmp6 in LSECs is phenocopied by erythrocyte lysis upon phenylhydrazine and elicits a distinct transcriptional signature compared to iron. Collectively, we identify LSECs as key Hb scavengers, a function that establishes the spleen-to-liver axis for iron recycling and contributes to heme detoxification during hemolysis.
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Registered trials
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