Evidence map›Paper›PMID 39196061›Full record

ArticleNature cardiovascular research2023

Cell-intrinsic effects of clonal hematopoiesis in heart failure.

Wesley T Abplanalp, Bianca Schuhmacher, Sebastian Cremer, Maximilian Merten, Mariana Shumliakivska, Igor Macinkovic, Andreas M Zeiher, David John, Stefanie Dimmeler

Abstract read
In one paragraph

Article in Nature cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed.

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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.

Wesley T Abplanalp *Institute of Cardiovascular Regeneration, Goethe University, Frankfurt, Germany.ORCID 0000-0001-5996-8997
Bianca Schuhmacher *Institute of Cardiovascular Regeneration, Goethe University, Frankfurt, Germany.
Sebastian CremerInstitute of Cardiovascular Regeneration, Goethe University, Frankfurt, Germany.
Maximilian MertenInstitute of Cardiovascular Regeneration, Goethe University, Frankfurt, Germany.
Mariana ShumliakivskaInstitute of Cardiovascular Regeneration, Goethe University, Frankfurt, Germany.
Igor MacinkovicInstitute of Cardiovascular Regeneration, Goethe University, Frankfurt, Germany.
Andreas M ZeiherInstitute of Cardiovascular Regeneration, Goethe University, Frankfurt, Germany.ORCID 0000-0003-1711-5819
David JohnInstitute of Cardiovascular Regeneration, Goethe University, Frankfurt, Germany.ORCID 0000-0003-3217-5449
Stefanie DimmelerInstitute of Cardiovascular Regeneration, Goethe University, Frankfurt, Germany. dimmeler@em.uni-frankfurt.de.ORCID 0000-0002-1045-2436

Funding

EC | EC Seventh Framework Programm | FP7 Ideas: European Research Council (FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013)) ERC-2021-ADG
6 · The paper itself

Abstract

Clonal hematopoiesis of indeterminate potential (CHIP) is caused by somatic mutations in hematopoietic stem cells and associates with worse prognosis in patients with heart failure. Patients harboring CHIP mutations show enhanced inflammation. However, whether these signatures are derived from the relatively low number of cells harboring mutations or are indicators of systemic pro-inflammatory activation that is associated with CHIP is unclear. Here we assess the cell-intrinsic effects of CHIP mutant cells in patients with heart failure. Using an improved single-cell sequencing pipeline (MutDetect-Seq), we show that DNMT3A mutant monocytes, CD4+ T cells and NK cells exhibit altered gene expression profiles. While monocytes showed increased genes associated with inflammation and phagocytosis, T cells and NK cells present increased activation signatures and effector functions. Increased paracrine signaling pathways are predicted and validated between mutant and wild-type monocytes and T cells, which amplify inflammatory circuits. Altogether, these data provide novel insights into how CHIP might promote a worse prognosis in patients with heart failure.

Indexed as

CD4-Positive T-LymphocytesClonal HematopoiesisDNA Methyltransferase 3AHeart FailureMonocytesMutationAgedDNA (Cytosine-5-)-MethyltransferasesFemaleHematopoietic Stem CellsHumansKiller Cells, NaturalMaleMiddle AgedParacrine CommunicationPhagocytosisDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNMT3A protein, human

Identifiers

PMID39196061
PMCPMC11357996

What Socratic holds

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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.