Evidence map›Paper›PMID 21935422›Full record

ArticlePloS one2011

Systemic maternal inflammation and neonatal hyperoxia induces remodeling and left ventricular dysfunction in mice.

Markus Velten, Kirk R Hutchinson, Matthew W Gorr, Loren E Wold, Pamela A Lucchesi, Lynette K Rogers

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.6field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Cannabidiol Protects the Neonatal Mouse Heart from Hyperoxia-Induced Injury.International journal of molecular sciences · 2025
    Article
  3. Perinatal Inflammation Results in Sex-Dependent Cardiac Dysfunction.Journal of cardiovascular development and disease · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Understanding the preterm human heart: What do we know so far?Anatomical record (Hoboken, N.J. : 2007) · 2022
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Perinatal inflammation induces sex-related differences in cardiovascular morbidities in mice.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  14. Long-term pulmonary and cardiovascular morbidities of neonatal hyperoxia exposure in mice.The international journal of biochemistry & cell biology · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. DHA suppresses chronic apoptosis in the lung caused by perinatal inflammation.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
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 2 institutions in 1 country.

Markus VeltenCenter for Perinatal Research, The Research Institute at Nationwide Children's Hospital, Department of Pediatrics, The Ohio State University, Columbus, Ohio, United States of America. Markus.Velten@NationwideChildrens.org
Kirk R Hutchinson
Matthew W Gorr
Loren E Wold
Pamela A Lucchesi
Lynette K Rogers
Nationwide Children's Hospital · USThe Ohio State University · US

Funding

Synergistic effects of obesity and air pollution on cardiac functionR01ES019923 · NIEHS · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI WOLD, LOREN EUGENE · 2011 to 2015
$1.8M
NHLBI NIH HHS 2R01-HL5604NIEHS NIH HHS R01 ES019923
6 · The paper itself

Abstract

aimsThe impact of the neonatal environment on the development of adult cardiovascular disease is poorly understood. Systemic maternal inflammation is linked to growth retardation, preterm birth, and maturation deficits in the developing fetus. Often preterm or small-for-gestational age infants require medical interventions such as oxygen therapy. The long-term pathological consequences of medical interventions on an immature physiology remain unknown. In the present study, we hypothesized that systemic maternal inflammation and neonatal hyperoxia exposure compromise cardiac structure, resulting in LV dysfunction during adulthood. METHODS AND

resultsPregnant C3H/HeN mice were injected on embryonic day 16 (E16) with LPS (80 µg/kg; i.p.) or saline. Offspring were placed in room air (RA) or 85% O(2) for 14 days and subsequently maintained in RA. Cardiac echocardiography, cardiomyocyte contractility, and molecular analyses were performed. Echocardiography revealed persistent lower left ventricular fractional shortening with greater left ventricular end systolic diameter at 8 weeks in LPS/O(2) than in saline/RA mice. Isolated cardiomyocytes from LPS/O(2) mice had slower rates of contraction and relaxation, and a slower return to baseline length than cardiomyocytes isolated from saline/RA controls. α-/β-MHC ratio was increased and Connexin-43 levels decreased in LPS/O(2) mice at 8 weeks. Nox4 was reduced between day 3 and 14 and capillary density was lower at 8 weeks of life in LPS/O(2) mice.

conclusionThese results demonstrate that systemic maternal inflammation combined with neonatal hyperoxia exposure induces alterations in cardiac structure and function leading to cardiac failure in adulthood and supports the importance of the intrauterine and neonatal milieu on adult health.

Indexed as

AnimalsAnimals, NewbornBody WeightCells, CulturedConnexinsEchocardiographyFemaleHeart VentriclesHyperoxiaImmunohistochemistryInflammationMajor Histocompatibility ComplexMaleMiceMyocardiumMyocytes, Cardiacconnexin 42ConnexinsNADPH Oxidase 4NADPH OxidasesNox4 protein, mouseVascular Endothelial Growth Factor AVentricular Myosins

Identifiers

PMID21935422
PMCPMC3173376
OpenAlexW2023795777

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Registered trials

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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.