Evidence map›Paper›PMID 38682236›Full record

ArticleAmerican journal of physiology. Cell physiology2024

Hemoglobin scavenger receptor CD163 as a potential biomarker of hemolysis-induced hepatobiliary injury in sickle cell disease.

Tomasz W Kaminski, Ayyanar Sivanantham, Anna Mozhenkova, Ashley Smith, Ramakrishna Ungalara, Rikesh K Dubey, Bibhav Shrestha, Corrine Hanway, Omika Katoch, Jesús Tejero and 4 more

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
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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

14 authors.

Tomasz W KaminskiThrombosis and Hemostasis Program, Versiti Blood Research Institute, Milwaukee, Wisconsin, United States.ORCID 0000-0002-8688-4171
Ayyanar SivananthamThrombosis and Hemostasis Program, Versiti Blood Research Institute, Milwaukee, Wisconsin, United States.
Anna MozhenkovaTransfusion Medicine, Vascular Biology and Cell Therapy Program, Versiti Blood Research Institute, Milwaukee, Wisconsin, United States.
Ashley SmithTransfusion Medicine, Vascular Biology and Cell Therapy Program, Versiti Blood Research Institute, Milwaukee, Wisconsin, United States.
Ramakrishna UngalaraPittsburgh Heart, Lung and Blood Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States.
Rikesh K DubeyThrombosis and Hemostasis Program, Versiti Blood Research Institute, Milwaukee, Wisconsin, United States.
Bibhav ShresthaTransfusion Medicine, Vascular Biology and Cell Therapy Program, Versiti Blood Research Institute, Milwaukee, Wisconsin, United States.
Corrine HanwayPittsburgh Heart, Lung and Blood Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States.
Omika KatochTransfusion Medicine, Vascular Biology and Cell Therapy Program, Versiti Blood Research Institute, Milwaukee, Wisconsin, United States.
Jesús TejeroPittsburgh Heart, Lung and Blood Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States.ORCID 0000-0003-3245-9978
Prithu SunddThrombosis and Hemostasis Program, Versiti Blood Research Institute, Milwaukee, Wisconsin, United States.
Enrico M NovelliPittsburgh Heart, Lung and Blood Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States.ORCID 0000-0003-3010-8285
Gregory J KatoPittsburgh Heart, Lung and Blood Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States.
Tirthadipa Pradhan-SunddTransfusion Medicine, Vascular Biology and Cell Therapy Program, Versiti Blood Research Institute, Milwaukee, Wisconsin, United States.ORCID 0000-0002-8763-4844

Funding

Pulmonary arteriole occlusion by platelet-neutrophil micro-emboli in Acute Chest SyndromeR01HL128297 · NHLBI · VERSITI WISCONSIN, INC. · PI SUNDD, PRITHU · 2015 to 2025
$5.4M
Mechanisms of platelet exosome-mediated acute chest syndrome in sickle cell diseaseR01HL141080 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI NEAL, MATTHEW D, NOVELLI, ENRICO M · 2019 to 2022
$3.1M
CD39-carrying extracellular vesicles regulate pulmonary thrombosis in Sickle Cell DiseaseR01HL166345 · NHLBI · VERSITI WISCONSIN, INC. · PI Prithu Sundd · 2023 to 2026
$3.1M
Molecular Mechanism of Sickle Cell Hepatic CrisisK01DK125617 · NIDDK · VERSITI WISCONSIN, INC. · PI PRADHAN-SUNDD, TIRTHADIPA · 2020 to 2024
$736k
American Heart Association (AHA) 18TPA34170588 and 23TPA1074022American Society of Hematology (ASH)HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL128297HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL141080HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL166345HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) NIH-NIDDK-125617NHLBI NIH HHS R01 HL128297NHLBI NIH HHS R01 HL141080NHLBI NIH HHS R01 HL166345NIDDK NIH HHS K01 DK125617
6 · The paper itself

Abstract

Sickle cell disease (SCD)-associated chronic hemolysis promotes oxidative stress, inflammation, and thrombosis leading to organ damage, including liver damage. Hemoglobin scavenger receptor CD163 plays a protective role in SCD by scavenging both hemoglobin-haptoglobin complexes and cell-free hemoglobin. A limited number of studies in the past have shown a positive correlation of CD163 expression with poor disease outcomes in patients with SCD. However, the role and regulation of CD163 in SCD-related hepatobiliary injury have not been fully elucidated yet. Here we show that chronic liver injury in SCD patients is associated with elevated levels of hepatic membrane-bound CD163. Hemolysis and increase in hepatic heme, hemoglobin, and iron levels elevate CD163 expression in the SCD mouse liver. Mechanistically we show that heme oxygenase-1 (HO-1) positively regulates membrane-bound CD163 expression independent of nuclear factor erythroid 2-related factor 2 (NRF2) signaling in SCD liver. We further demonstrate that the interaction between CD163 and HO-1 is not dependent on CD163-hemoglobin binding. These findings indicate that CD163 is a potential biomarker of SCD-associated hepatobiliary injury. Understanding the role of HO-1 in membrane-bound CD163 regulation may help identify novel therapeutic targets for hemolysis-induced chronic liver injury.

Indexed as

Anemia, Sickle CellAntigens, CDAntigens, Differentiation, MyelomonocyticBiomarkersHeme Oxygenase-1HemoglobinsHemolysisReceptors, Cell SurfaceAdultAnimalsCD163 AntigenFemaleHaptoglobinsHemeHumansLiverAntigens, CDAntigens, Differentiation, MyelomonocyticBiomarkersCD163 AntigenHaptoglobinsHemeHeme Oxygenase-1HemoglobinsHMOX1 protein, humanHmox1 protein, mouseMembrane ProteinsNF-E2-Related Factor 2Receptors, Cell SurfaceCD163hemoglobin clearancehemolysisHO-1sickle cell disease

Identifiers

PMID38682236
PMCPMC11427010

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.