Evidence map›Paper›PMID 33804125›Full record

ArticleCells2021

Heme Oxygenase-1 Contributes to Both the Engulfment and the Anti-Inflammatory Program of Macrophages during Efferocytosis.

Éva Fige, Judit Szendrei, László Sós, Izabela Kraszewska, László Potor, József Balla, Zsuzsa Szondy

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Éva FigeSection of Dental Biochemistry, Department of Biochemistry and Molecular Biology, Faculty of Dentistry, University of Debrecen, 4012 Debrecen, Hungary.
Judit SzendreiSection of Dental Biochemistry, Department of Biochemistry and Molecular Biology, Faculty of Dentistry, University of Debrecen, 4012 Debrecen, Hungary.
László SósSection of Dental Biochemistry, Department of Biochemistry and Molecular Biology, Faculty of Dentistry, University of Debrecen, 4012 Debrecen, Hungary.
Izabela KraszewskaDepartment of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, 30-387 Krakow, Poland.
László PotorHAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian Academy of Sciences, University of Debrecen, 4012 Debrecen, Hungary.
József BallaHAS-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian Academy of Sciences, University of Debrecen, 4012 Debrecen, Hungary.
Zsuzsa SzondySection of Dental Biochemistry, Department of Biochemistry and Molecular Biology, Faculty of Dentistry, University of Debrecen, 4012 Debrecen, Hungary.ORCID 0000-0001-8347-9552
University of Debrecen · HUJagiellonian University · PL

Funding

EFOP-3.4.2-VEKOP 15-2015-00001EFOP-3.6.3-VEKOP 16-2017-0009GINOP- 2.3.2-15-2016-00006National Research, Development and Innovation Office, Hungary 124244
6 · The paper itself

Abstract

Heme oxygenase-1 (HO-1) plays a vital role in the catabolism of heme and yields equimolar amounts of biliverdin, carbon monoxide, and free iron. We report that macrophages engulfing either the low amount of heme-containing apoptotic thymocytes or the high amount of heme-containing eryptotic red blood cells (eRBCs) strongly upregulate HO-1. The induction by apoptotic thymocytes is dependent on soluble signals, which do not include adenylate cyclase activators but induce the p38 mitogen-activated protein (MAP) kinase pathway, while in the case of eRBCs, it is cell uptake-dependent. Both pathways might involve the regulation of BTB and CNC homology 1 (BACH1), which is the repressor transcription regulator factor of the HO-1 gene. Long-term continuous efferocytosis of apoptotic thymocytes is not affected by the loss of HO-1, but that of eRBCs is inhibited. This latter is related to an internal signaling pathway that prevents the efferocytosis-induced increase in Rac1 activity. While the uptake of apoptotic cells suppressed the basal pro-inflammatory cytokine production in wild-type macrophages, in the absence of HO-1, engulfing macrophages produced enhanced amounts of pro-inflammatory cytokines. Our data demonstrate that HO-1 is required for both the engulfment and the anti-inflammatory response parts of the efferocytosis program.

Indexed as

AnimalsAnti-Inflammatory AgentsGene Expression RegulationHeme Oxygenase-1InflammationMacrophagesMiceMice, Inbred C57BLNF-E2-Related Factor 2PhagocytosisSignal TransductionUp-RegulationAnti-Inflammatory AgentsHeme Oxygenase-1NF-E2-Related Factor 2adenosine A2A receptorBACH1efferocytosisheme oxygenase-1inflammation

Identifiers

PMID33804125
PMCPMC8001822
OpenAlexW3137306820

What OpenQuestion holds

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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 OpenQuestion graph.