Evidence map›Paper›PMID 29664678›Full record

ArticleAmerican journal of respiratory and critical care medicine2018

Endothelial and Smooth Muscle Cell Interaction via FoxM1 Signaling Mediates Vascular Remodeling and Pulmonary Hypertension.

Zhiyu Dai, Maggie M Zhu, Yi Peng, Hua Jin, Narsa Machireddy, Zhijian Qian, Xianming Zhang, You-Yang Zhao

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

95 citing papers in PubMed, 179 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. BMP9 regulates the endothelial secretome to drive pulmonary hypertension.bioRxiv : the preprint server for biology · 2025
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  13. Review
  14. Mechanisms of lung endothelial cell injury and survival in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

35 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Zhiyu Dai1 Program for Lung and Vascular Biology, Stanley Manne Children's Research Institute, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois.ORCID 0000-0002-2945-7923
Maggie M Zhu1 Program for Lung and Vascular Biology, Stanley Manne Children's Research Institute, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois.
Yi Peng1 Program for Lung and Vascular Biology, Stanley Manne Children's Research Institute, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois.
Hua Jin1 Program for Lung and Vascular Biology, Stanley Manne Children's Research Institute, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois.
Narsa Machireddy1 Program for Lung and Vascular Biology, Stanley Manne Children's Research Institute, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois.
Zhijian Qian5 Department of Medicine, Division of Hematology/Oncology, University of Illinois at Chicago, Chicago, Illinois.
Xianming Zhang1 Program for Lung and Vascular Biology, Stanley Manne Children's Research Institute, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois.
You-Yang Zhao1 Program for Lung and Vascular Biology, Stanley Manne Children's Research Institute, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois.
Lurie Children's Hospital · USNorthwestern University · USUniversity of Illinois Chicago · US

Funding

Trpm2 Regulation of Phagocyte Bactericidal Activity and Resolution of Lung InjuryP01HL077806 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ZHAO, YOU-YANG · 2005 to 2019
$27.0M
Pulmonary Hypertension Breakthrough InitiativeR24HL123767 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ALDRED, MICHEALA A, ERZURUM, SERPIL C. · 2014 to 2017
$10.1M
Novel mechanisms of obliterative pulmonary vascular remodeling and sever pulmonary arterial hypertensionR01HL133951 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ZHAO, YOU-YANG · 2016 to 2024
$4.9M
Repair mechanisms of sepsis induced endothelial dysfunction and lung injuryR01HL125350 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MALIK, ASRAR B., ZHAO, YOU-YANG · 2014 to 2018
$3.2M
Novel Signalings and Molecular Targets Of Endothelial Regeneration In Aging LungR01HL123957 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ZHAO, YOU-YANG · 2014 to 2018
$2.0M
The role of EVI1-induced hypermethylation in leukemogenesis.R01HL131444 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI QIAN, ZHIJIAN · 2016 to 2019
$1.6M
Role of Smooth Muscle Progenitor Cells in Obliterative Vascular Remodeling and PHK99HL138278 · NHLBI · LURIE CHILDREN'S HOSPITAL OF CHICAGO · PI DAI, ZHIYU · 2017 to 2018
$265k
NHLBI NIH HHS K99 HL138278NHLBI NIH HHS P01 HL077806NHLBI NIH HHS R01 HL123957NHLBI NIH HHS R01 HL125350NHLBI NIH HHS R01 HL131444NHLBI NIH HHS R01 HL133951NHLBI NIH HHS R24 HL123767
6 · The paper itself

Abstract

rationaleAngioproliferative vasculopathy is a hallmark of pulmonary arterial hypertension (PAH). However, little is known about how endothelial cell (EC) and smooth muscle cell (SMC) crosstalk regulates the angioproliferative vascular remodeling.

objectivesTo investigate the role of EC and SMC interaction and underlying signaling pathways in pulmonary hypertension (PH) development.

methodsSMC-specific Foxm1 (forkhead box M1) or Cxcr4 knockout mice, EC-specific Foxm1 or Egln1 knockout mice, and EC-specific Egln1/Cxcl12 double knockout mice were used to assess the role of FoxM1 on SMC proliferation and PH. Lung tissues and cells from patients with PAH were used to validate clinical relevance. FoxM1 inhibitor thiostrepton was used in Sugen 5416/hypoxia- and monocrotaline-challenged rats. MEASUREMENTS AND MAIN

resultsFoxM1 expression was markedly upregulated in lungs and pulmonary arterial SMCs of patients with idiopathic PAH and four discrete PH rodent models. Mice with SMC- (but not EC-) specific deletion of Foxm1 were protected from hypoxia- or Sugen 5416/hypoxia-induced PH. The upregulation of FoxM1 in SMCs induced by multiple EC-derived factors (PDGF-B, CXCL12, ET-1, and MIF) mediated SMC proliferation. Genetic deletion of endothelial Cxcl12 in Egln1

conclusionsMultiple factors derived from dysfunctional ECs induced FoxM1 expression in SMCs and activated FoxM1-dependent SMC proliferation, which contributes to pulmonary vascular remodeling and PH. Thus, targeting FoxM1 signaling represents a novel strategy for treatment of idiopathic PAH.

Indexed as

Vascular RemodelingAnimalsEndothelium, VascularForkhead Box Protein M1HumansHypertension, PulmonaryMiceMice, KnockoutMuscle, Smooth, VascularSignal TransductionForkhead Box Protein M1Foxm1 protein, mouseCXCL12/CXCR4endothelial cellshyperproliferationpulmonary vascular remodelingsmooth muscle cells

Identifiers

PMID29664678
PMCPMC6222462
OpenAlexW2800049907

What Socratic holds

Textmetadata
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.