Evidence map›Paper›PMID 28855075›Full record

ReviewCytokine2017

Origin and production of inflammatory perivascular macrophages in pulmonary hypertension.

Jonathan Florentin, Partha Dutta

Open access · greenAbstract readReview
In one paragraph

Review in Cytokine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Identification of a distinct cluster of GDF15Frontiers in immunology · 2024
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Protective effect ofBioscience reports · 2019
    Article
  20. 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

2 authors at 1 institution in 1 country.

Jonathan FlorentinCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Partha DuttaCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: duttapa@pitt.edu.
University of Pittsburgh · US

Funding

Mechanisms of Myocardial Infarction-induced insulin resistanceR01HL143967 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DUTTA, PARTHA · 2018 to 2022
$2.6M
Effect of diabetes on myelopoiesis and atherosclerosisR00HL121076 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DUTTA, PARTHA · 2016 to 2018
$732k
NHLBI NIH HHS R00 HL121076NHLBI NIH HHS R01 HL143967
6 · The paper itself

Abstract

Myeloid cells, including monocytes and macrophages participate in steady state immune homeostasis and help mount the adaptive immune response during infection. The function and production of these cells in sterile inflammation, such as pulmonary hypertension (PH), is understudied. Emerging data indicate that pulmonary inflammation mediated by lung perivascular macrophages is a key pathogenic driver of pulmonary remodeling leading to increased right ventricular systolic pressure (RVSP). However, the origin of these macrophages in pulmonary inflammation is unknown. Inflammatory monocytes, the precursors of pathogenic macrophages, are derived from hematopoietic stem and progenitor cells (HSPC) in the bone marrow and spleen during acute and chronic inflammation. Understanding the role of these organs in monocytopoiesis, and the mechanisms of HSPC proliferation and differentiation in PH are important to discover therapeutic targets curbing inflammation. This review will summarize the current limited knowledge of the origin of lung macrophage subsets and over-production of inflammatory monocytes in PH.

Indexed as

AnimalsBlood PressureCell DifferentiationCell ProliferationHematopoietic Stem CellsHumansHypertension, PulmonaryMacrophagesMacrophages, AlveolarMiceMonocytesPneumoniaAlveolar macrophagesHSC progenitorsInflammationInterstitial macrophagesPulmonary hypertension

Identifiers

PMID28855075
PMCPMC5650934
OpenAlexW2751954658

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.