Evidence map›Paper›PMID 29069365›Full record

ReviewEuropean heart journal2018

Monocyte and haematopoietic progenitor reprogramming as common mechanism underlying chronic inflammatory and cardiovascular diseases.

Renate M Hoogeveen, Matthias Nahrendorf, Niels P Riksen, Mihai G Netea, Menno P J de Winther, Esther Lutgens, Børge G Nordestgaard, Michel Neidhart, Erik S G Stroes, Alberico L Catapano and 1 more

Erratum issuedOpen access · bronzeAbstract readReview
In one paragraph

Review in European heart journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 7 institutions in 5 countries.

Renate M HoogeveenDepartment of Vascular Medicine, Academic Medical Centre, Meibergdreef 9, Amsterdam, The Netherlands.
Matthias NahrendorfCenter for Systems Biology and Department of Imaging, Massachusetts General Hospital and Harvard Medical School, Boston, 55 Fruit Street Boston, MA, USA.
Niels P RiksenDepartment of Internal Medicine, Radboud University Medical Center, Geert Grooteplein Zuid 8, Nijmegen, The Netherlands.
Mihai G NeteaDepartment of Internal Medicine, Radboud University Medical Center, Geert Grooteplein Zuid 8, Nijmegen, The Netherlands.
Menno P J de WintherDepartment of Medical Biochemistry, Academic Medical Centre, Meibergdreef 9, Amsterdam, The Netherlands.
Esther LutgensInstitute for Cardiovascular Prevention (IPEK), Ludwig Maximilians University (LMU), Pettenkoferstraße 9, Munich, Germany.
Børge G NordestgaardThe Copenhagen General Population Study and Department of Clinical Biochemistry, Herlev and Gentofte Hospital, Copenhagen University Hospital, Ringvej 75, Herlev, Copenhagen, Denmark.
Michel NeidhartCenter of Experimental Rheumatology, University Hospital Zurich, Schlieren, Switzerland.
Erik S G StroesDepartment of Vascular Medicine, Academic Medical Centre, Meibergdreef 9, Amsterdam, The Netherlands.
Alberico L CatapanoDepartment of Pharmacological and Biomolecular Sciences, University of Milan and IRCCS Multimedica, Via Balzaretti, Milano, Italy.
Siroon BekkeringDepartment of Vascular Medicine, Academic Medical Centre, Meibergdreef 9, Amsterdam, The Netherlands.
Academic Medical Center · NLCenter for Systems Biology · USGentofte Hospital · DKLudwig-Maximilians-Universität München · DERadboud University Medical Center · NLRadboud University Nijmegen · NLUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large number of cardiovascular events are not prevented by current therapeutic regimens. In search for additional, innovative strategies, immune cells have been recognized as key players contributing to atherosclerotic plaque progression and destabilization. Particularly the role of innate immune cells is of major interest, following the recent paradigm shift that innate immunity, long considered to be incapable of learning, does exhibit immunological memory mediated via epigenetic reprogramming. Compelling evidence shows that atherosclerotic risk factors promote immune cell migration by pre-activation of circulating innate immune cells. Innate immune cell activation via metabolic and epigenetic reprogramming perpetuates a systemic low-grade inflammatory state in cardiovascular disease (CVD) that is also common in other chronic inflammatory disorders. This opens a new therapeutic area in which metabolic or epigenetic modulation of innate immune cells may result in decreased systemic chronic inflammation, alleviating CVD, and its co-morbidities.

Indexed as

Cellular ReprogrammingEpigenesis, GeneticImmunity, InnateAnimalsAtherosclerosisChronic DiseaseHematopoietic Stem CellsHumansImmunologic MemoryInflammationMonocytesMultimodal Imaging

Identifiers

PMID29069365
PMCPMC6174026
OpenAlexW2767099852

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.