Evidence map›Paper›PMID 38269586›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2024

Nonpreferential but Detrimental Accumulation of Macrophages With Clonal Hematopoiesis-Driver Mutations in Cardiovascular Tissues-Brief Report.

Tsai-Sang Dederichs, Assel Yerdenova, Hauke Horstmann, Tamara Antonela Vico, Simone Nübling, Rémi Peyronnet, Dietmar Pfeifer, Constantin von Zur Muehlen, Timo Heidt, Dennis Wolf and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

6 citing papers in PubMed, 11 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

13 authors at 2 institutions in 1 country.

Tsai-Sang DederichsDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine, University of Freiburg, Germany (T.-S.D., A.Y., H.H., T.A.V., C.v.z.M., T.H., D. Wolf, D. Westermann, I.H.).ORCID 0000-0001-8347-7987
Assel YerdenovaDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine, University of Freiburg, Germany (T.-S.D., A.Y., H.H., T.A.V., C.v.z.M., T.H., D. Wolf, D. Westermann, I.H.).
Hauke HorstmannDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine, University of Freiburg, Germany (T.-S.D., A.Y., H.H., T.A.V., C.v.z.M., T.H., D. Wolf, D. Westermann, I.H.).ORCID 0000-0002-9971-1800
Tamara Antonela VicoDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine, University of Freiburg, Germany (T.-S.D., A.Y., H.H., T.A.V., C.v.z.M., T.H., D. Wolf, D. Westermann, I.H.).ORCID 0000-0002-5428-688X
Simone NüblingInstitute for Experimental Cardiovascular Medicine, Cardio-Vascular Biobank, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine, University of Freiburg, Germany (S.N., R.P., I.H.).
Rémi PeyronnetInstitute for Experimental Cardiovascular Medicine, Cardio-Vascular Biobank, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine, University of Freiburg, Germany (S.N., R.P., I.H.).
Dietmar PfeiferDepartment of Internal Medicine I, Medical Center and Faculty of Medicine, University of Freiburg, Germany (D.P.).ORCID 0000-0003-2684-5944
Constantin von Zur MuehlenDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine, University of Freiburg, Germany (T.-S.D., A.Y., H.H., T.A.V., C.v.z.M., T.H., D. Wolf, D. Westermann, I.H.).
Timo HeidtDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine, University of Freiburg, Germany (T.-S.D., A.Y., H.H., T.A.V., C.v.z.M., T.H., D. Wolf, D. Westermann, I.H.).
Dennis WolfDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine, University of Freiburg, Germany (T.-S.D., A.Y., H.H., T.A.V., C.v.z.M., T.H., D. Wolf, D. Westermann, I.H.).ORCID 0000-0003-1525-4348
Martin CzernyDepartment of Cardiovascular Surgery, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine University of Freiburg, Germany (M.C.).
Dirk WestermannDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine, University of Freiburg, Germany (T.-S.D., A.Y., H.H., T.A.V., C.v.z.M., T.H., D. Wolf, D. Westermann, I.H.).ORCID 0000-0002-7542-1956
Ingo HilgendorfDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen and Faculty of Medicine, University of Freiburg, Germany (T.-S.D., A.Y., H.H., T.A.V., C.v.z.M., T.H., D. Wolf, D. Westermann, I.H.).ORCID 0000-0002-0024-1643
University of Freiburg · DEUniversitäts-Herzzentrum Freiburg-Bad Krozingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClonal hematopoiesis of indeterminate potential (CHIP) is an acquired genetic risk factor for both leukemia and cardiovascular disease. It results in proinflammatory myeloid cells in the bone marrow and blood; however, how these cells behave in the cardiovascular tissue remains unclear. Our study aimed at investigating whether CHIP-mutated macrophages accumulate preferentially in cardiovascular tissues and examining the transcriptome of tissue macrophages from

methodsWe recruited patients undergoing carotid endarterectomy or heart surgeries to screen for CHIP mutation carriers using targeted genomic sequencing. Myeloid and lymphoid cells were isolated from blood and cardiovascular tissue collected during surgeries using flow cytometry. DNA and RNA extracted from these sorted cells were subjected to variant allele frequency measurement using droplet digital polymerase chain reaction and transcriptomic profiling using bulk RNA sequencing, respectively.

resultsUsing droplet digital polymerase chain reaction, we detected similar variant allele frequency of CHIP in monocytes from blood and macrophages from atheromas and heart tissues, even among heart macrophages with and without CCR2 (C-C motif chemokine receptor 2) expression. Bulk RNA sequencing revealed a proinflammatory gene profile of myeloid cells from

conclusionsQuantitatively, CHIP-mutated myeloid cells did not preferentially accumulate in cardiovascular tissues, but qualitatively, they expressed a more disease-prone phenotype.

Indexed as

Cardiovascular DiseasesClonal HematopoiesisHematopoiesisHumansMacrophagesMutationclonal hematopoiesisheart disease risk factorsinflammationmacrophages

Identifiers

PMID38269586
PMCPMC10880934
OpenAlexW4391225231

What Socratic 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 Socratic graph.