Evidence map›Paper›PMID 19423843›Full record

ArticleCirculation research2009

Inhibition of the SDF-1/CXCR4 axis attenuates neonatal hypoxia-induced pulmonary hypertension.

Karen C Young, Eneida Torres, Konstantinos E Hatzistergos, Dorothy Hehre, Cleide Suguihara, Joshua M Hare

Open access · greenAbstract read
In one paragraph

Article in Circulation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

57 citing papers in PubMed, 101 citations in OpenAlex.

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  16. Cytokines, Chemokines, and Inflammation in Pulmonary Arterial Hypertension.Advances in experimental medicine and biology · 2021
    Article
  17. Article
  18. Mural Cell SDF1 Signaling Is Associated with the Pathogenesis of Pulmonary Arterial Hypertension.American journal of respiratory cell and molecular biology · 2020
    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

6 authors at 1 institution in 1 country.

Karen C YoungDepartment of Pediatrics/Division of Neonatology, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Eneida Torres
Konstantinos E Hatzistergos
Dorothy Hehre
Cleide Suguihara
Joshua M Hare
Stem Cell Institute · PA

Funding

Mesenchymal Stem Cell CardiomyoplastyU54HL081028 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI HARE, JOSHUA M · 2005 to 2009
$12.1M
Cellular Cardiomyoplasty for Chronic Heart FailureR01HL084275 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2007 to 2016
$3.8M
OXIDATIVE STRESS IN HEART FAILURE: MECHANISMSR01HL065455 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2000 to 2008
$2.6M
Nitroso/redox balance in myocardial infarctionR01HL094849 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2009 to 2013
$2.2M
Aging impairs stem-cell mediated myocardial repairR01AG025017 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARE, JOSHUA M · 2004 to 2008
$1.5M
The Role of c-kit in the Pathogenesis of Neonatal Pulmonary HypertensionK08HL097067 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI YOUNG, KAREN CECILE · 2009 to 2013
$612k
NHLBI NIH HHS HL-084275NHLBI NIH HHS HL-094849NHLBI NIH HHS HL-65455NHLBI NIH HHS K08 HL097067NHLBI NIH HHS R01 HL065455NHLBI NIH HHS R01 HL084275NHLBI NIH HHS R01 HL094849NHLBI NIH HHS U54 HL081028NHLBI NIH HHS U54HL-081028NIA NIH HHS AG-025017NIA NIH HHS R01 AG025017
6 · The paper itself

Abstract

Exposure of the neonatal lung to chronic hypoxia produces significant pulmonary vascular remodeling, right ventricular hypertrophy, and decreased lung alveolarization. Given recent data suggesting that stem cells could contribute to pulmonary vascular remodeling and right ventricular hypertrophy, we tested the hypothesis that blockade of SDF-1 (stromal cell-derived factor 1), a key stem cell mobilizer or its receptor, CXCR4 (CXC chemokine receptor 4), would attenuate and reverse hypoxia-induced cardiopulmonary remodeling in newborn mice. Neonatal mice exposed to normoxia or hypoxia were randomly assigned to receive daily intraperitoneal injections of normal saline, AMD3100, or anti-SDF-1 antibody from postnatal day 1 to 7 (preventive strategy) or postnatal day 7 to 14 (therapeutic strategy). As compared to normal saline, inhibition of the SDF-1/CXCR4 axis significantly improved lung alveolarization and decreased pulmonary hypertension, right ventricular hypertrophy, vascular remodeling, vascular cell proliferation, and lung or right ventricular stem cell expressions to near baseline values. We therefore conclude that the SDF-1/CXCR4 axis both prevents and reverses hypoxia-induced cardiopulmonary remodeling in neonatal mice, by decreasing progenitor cell recruitment to the pulmonary vasculature, as well as by decreasing pulmonary vascular cell proliferation. These data offer novel insights into the role of the SDF-1/CXCR4 axis in the pathogenesis of neonatal hypoxia-induced cardiopulmonary remodeling and have important therapeutic implications.

Indexed as

AnimalsAnimals, NewbornBenzylaminesBone Marrow CellsChemokine CXCL12CyclamsHeart VentriclesHeterocyclic CompoundsHumansHypertension, PulmonaryHypoxiaInfant, NewbornInfant, PrematureMicePulmonary CirculationReceptors, CXCR4BenzylaminesChemokine CXCL12CXCR4 protein, humanCXCR4 protein, mouseCyclamsHeterocyclic CompoundsplerixaforReceptors, CXCR4

Identifiers

PMID19423843
PMCPMC2757744
OpenAlexW1969554913

What OpenQuestion holds

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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.