Evidence map›Paper›PMID 32849588›Full record

ArticleFrontiers in immunology2020

Hemopexin as an Inhibitor of Hemolysis-Induced Complement Activation.

Victoria Poillerat, Thomas Gentinetta, Juliette Leon, Andreas Wassmer, Monika Edler, Carine Torset, Dandan Luo, Gerald Tuffin, Lubka T Roumenina

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  8. Hemopexin reverses activation of lung eIF2α and decreases mitochondrial injury in chlorine-exposed mice.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  9. Article
  10. Accelerated atherosclerosis in beta-thalassemia.American journal of physiology. Heart and circulatory physiology · 2023
    Article
  11. Inflammation alters iron distribution in bone and spleen in mice.Metallomics : integrated biometal science · 2023
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  13. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 3 countries.

Victoria PoilleratCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université de Paris, Paris, France.
Thomas GentinettaCSL Behring AG, Bern, Switzerland.
Juliette LeonCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université de Paris, Paris, France.
Andreas WassmerCSL Behring AG, Bern, Switzerland.
Monika EdlerCSL Behring AG, Bern, Switzerland.
Carine TorsetCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université de Paris, Paris, France.
Dandan LuoCSL Behring, King of Prussia, PA, United States.
Gerald TuffinCSL Behring AG, Bern, Switzerland.
Lubka T RoumeninaCentre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université de Paris, Paris, France.
CSL (Switzerland) · CHCentre de Recherche des Cordeliers · FRCSL (United States) · USInserm · FRSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hemopexin is the main plasmatic scavenger of cell-free heme, released in the context of intravascular hemolysis or major cell injury. Heme is indispensable for the oxygen transport by hemoglobin but when released outside of the erythrocytes it becomes a danger-associated molecular pattern, contributing to tissue injury. One of the mechanisms of pro-inflammatory action of heme is to activate the innate immune complement cascade. Therefore, we hypothesized that injection of hemopexin will prevent hemolysis-induced complement activation. Human plasma-derived hemopexin is compatible with the heme clearance machinery of the mice. 100 or 500 mg/kg of hemopexin was injected in C57Bl/6 mice before treatment with phenylhydrazine (inducer of erythrocytes lysis) or with PBS as a control. Blood was taken at different timepoints to determine the pharmacokinetic of injected hemopexin in presence and absence of hemolysis. Complement activation was determined in plasma, by the C3 cleavage (western blot) and in the kidneys (immunofluorescence). Kidney injury was evaluated by urea and creatinine in plasma and renal NGAL and HO-1 gene expression were measured. The pharmacokinetic properties of hemopexin (mass spectrometry) in the hemolytic mice were affected by the target-mediated drug disposition phenomenon due to the high affinity of binding of hemopexin to heme. Hemolysis induced complement overactivation and signs of mild renal dysfunction at 6 h, which were prevented by hemopexin, except for the NGAL upregulation. The heme-degrading capacity of the kidney, measured by the HO-1 expression, was not affected by the treatment. These results encourage further studies of hemopexin as a therapeutic agent in models of diseases with heme overload.

Indexed as

AnimalsComplement ActivationHemolysisHemopexinHumansKidneyMiceMice, Inbred C57BLHemopexinC3complementhemehemolysishemopexinkidney injury

Identifiers

PMID32849588
PMCPMC7412979
OpenAlexW3046362022

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Registered trials

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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.