Evidence map›Paper›PMID 34172720›Full record

ArticleNature communications2021

Post-myocardial infarction heart failure dysregulates the bone vascular niche.

Jedrzej Hoffmann, Guillermo Luxán, Wesley Tyler Abplanalp, Simone-Franziska Glaser, Tina Rasper, Ariane Fischer, Marion Muhly-Reinholz, Michael Potente, Birgit Assmus, David John and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  4. NF-Frontiers in cardiovascular medicine · 2026
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  7. Article
  8. Article
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  10. Article
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  13. The heart-bone connection: relationships between myocardial infarction and osteoporotic fracture.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  14. Review
  15. Article
  16. Review
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  19. 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

12 authors at 2 institutions in 1 country.

Jedrzej Hoffmann *Department of Cardiology, Center of Internal Medicine, Goethe University Frankfurt, Frankfurt, Germany.ORCID 0000-0003-0487-4373
Guillermo Luxán *German Center for Cardiovascular Research DZHK, Frankfurt am Main, Germany.ORCID 0000-0001-8350-8659
Wesley Tyler Abplanalp *German Center for Cardiovascular Research DZHK, Frankfurt am Main, Germany.
Simone-Franziska GlaserGerman Center for Cardiovascular Research DZHK, Frankfurt am Main, Germany.ORCID 0000-0002-0808-2659
Tina RasperInstitute of Cardiovascular Regeneration, Center of Molecular Medicine, Goethe University Frankfurt, Frankfurt, Germany.
Ariane FischerInstitute of Cardiovascular Regeneration, Center of Molecular Medicine, Goethe University Frankfurt, Frankfurt, Germany.
Marion Muhly-ReinholzInstitute of Cardiovascular Regeneration, Center of Molecular Medicine, Goethe University Frankfurt, Frankfurt, Germany.
Michael PotenteAngiogenesis and Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Birgit AssmusDepartment of Cardiology, Center of Internal Medicine, Goethe University Frankfurt, Frankfurt, Germany.
David JohnGerman Center for Cardiovascular Research DZHK, Frankfurt am Main, Germany.
Andreas Michael ZeiherDepartment of Cardiology, Center of Internal Medicine, Goethe University Frankfurt, Frankfurt, Germany.
Stefanie DimmelerGerman Center for Cardiovascular Research DZHK, Frankfurt am Main, Germany. Dimmeler@em.uni-frankfurt.de.ORCID 0000-0002-1045-2436
Goethe University Frankfurt · DEMax Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The regulation of bone vasculature by chronic diseases, such as heart failure is unknown. Here, we describe the effects of myocardial infarction and post-infarction heart failure on the bone vascular cell composition. We demonstrate an age-independent loss of type H endothelium in heart failure after myocardial infarction in both mice and humans. Using single-cell RNA sequencing, we delineate the transcriptional heterogeneity of human bone marrow endothelium, showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure. Endothelial-specific overexpression of MYC was sufficient to induce type H bone endothelial cells, whereas inhibition of NLRP3-dependent IL-1β production partially prevented the post-myocardial infarction loss of type H vasculature in mice. These results provide a rationale for using anti-inflammatory therapies to prevent or reverse the deterioration of bone vascular function in ischemic heart disease.

Indexed as

AgedAnimalsBone and BonesCase-Control StudiesEndothelial CellsFemaleFuransGenes, mycHeart FailureHematopoietic Stem CellsHumansIndenesInflammationInterleukin-1betaMaleMiceFuransIL1B protein, humanIndenesInterleukin-1betaN-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamidePECAM1 protein, humanPlatelet Endothelial Cell Adhesion Molecule-1Sulfonamides

Identifiers

PMID34172720
PMCPMC8233308
OpenAlexW3176717306

What OpenQuestion 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 OpenQuestion graph.