Evidence map›Paper›PMID 30585362›Full record

ReviewJournal of internal medicine2019

Myeloid cells in cardiovascular organs.

M Nahrendorf

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of internal medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. The Impact of Exercise on Immunity, Metabolism, and Atherosclerosis.International journal of molecular sciences · 2023
    Review
  6. Quo Vadis? Immunodynamics of Myeloid Cells after Myocardial Infarction.International journal of molecular sciences · 2022
    Review
  7. Interleukin 4/13 signaling in cardiac regeneration and repair.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  8. Review
  9. Review
  10. Review
  11. Macrophage Plasticity and Atherosclerosis Therapy.Frontiers in molecular biosciences · 2021
    Review
  12. Review
  13. Article
  14. Review
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

1 author at 1 institution in 1 country.

M NahrendorfCenter for Systems Biology and Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-4021-1887
Harvard University · US

Funding

Imaging organ system interfaces in ischemic heart diseaseR35HL139598 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS · 2018 to 2024
$6.9M
Skull marrow crosstalk with the central nervous systemR01NS108419 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MOSKOWITZ, MICHAEL A., NAHRENDORF, MATTHIAS · 2018 to 2022
$3.4M
Lifestyle effects on hematopoiesis and atherosclerosisR01HL128264 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS, SWIRSKI, FILIP K · 2015 to 2018
$3.3M
Dynamic interactions between ischemic stroke, immunity and the bone marrowR01NS084863 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MOSKOWITZ, MICHAEL A., NAHRENDORF, MATTHIAS · 2014 to 2018
$3.2M
PET/MRI of cardiac repairR01HL096576 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS · 2009 to 2017
$2.8M
Quantitative nanoparticle imaging of macrophagesR01HL131495 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS, WEISSLEDER, MD, PHD, RALPH · 2017 to 2020
$2.7M
Anti-inflammatory nanoparticle formulations to treat atherosclerosisR01HL118440 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MULDER, WILLEM, NAHRENDORF, MATTHIAS · 2014 to 2017
$2.3M
Interfering with the macrophage life cycle of atherosclerosisR01HL125428 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ANDERSON, DANIEL G, NAHRENDORF, MATTHIAS · 2017 to 2020
$1.9M
Cell-Cell Interaction in Heart FailureR01HL117829 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS · 2014 to 2017
$1.7M
NHLBI NIH HHS R01 HL096576NHLBI NIH HHS R01 HL117829NHLBI NIH HHS R01 HL118440NHLBI NIH HHS R01 HL125428NHLBI NIH HHS R01 HL128264NHLBI NIH HHS R01 HL131495NHLBI NIH HHS R35 HL139598NINDS NIH HHS R01 NS084863NINDS NIH HHS R01 NS108419
6 · The paper itself

Abstract

Myeloid cells assume a wide range of phenotypes, some of which are protective against injury and infection whilst others promote cardiovascular disease. This heterogeneity is partially caused by switching of cell sources from local tissue-resident macrophage proliferation to recruitment of circulating cells, and partially due to macrophages' phenotypic plasticity. While long-lived tissue-resident macrophages support development, tissue homoeostasis and cardiac conduction, monocyte-derived cells may promote destruction of the arterial wall and the myocardium, leading to organ ischaemia and heart failure. Influencing myeloid cell flux and phenotype shifts emerges as a therapeutic opportunity in many disease areas, including atherosclerosis, acute myocardial infarction, heart failure and stroke. However, it is currently unclear which cell subsets and drug targets are the most efficient and safest options. Here I review the neutrophil and macrophage supply chain and the cells' emerging heterogeneity in the setting of atherosclerosis and ischaemic heart disease.

Indexed as

AtherosclerosisCardiovascular DiseasesHumansMyeloid CellsMyocardial Ischemiaatherosclerosismacrophagemonocytemyocardial infarctionneutrophil

Identifiers

PMID30585362
PMCPMC6497541
OpenAlexW2906403714

What OpenQuestion holds

Textmetadata
LicenceTDM
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.