Evidence map›Paper›PMID 20712587›Full record

ReviewCurrent molecular medicine2010

Hypoxia and fetal heart development.

A J Patterson, L Zhang

Open access · bronzeAbstract readReview
In one paragraph

Review in Current molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
16.5field-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

112 citing papers in PubMed, 233 citations in OpenAlex.

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

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.

A J PattersonCenter for Perinatal Biology, Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA. apatterson@llu.edu
L Zhang
Loma Linda University · US

Funding

Uterine vascular responses to pregnancy and long term hypoxemiaP01HD031226 · NICHD · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 1995 to 2014
$21.4M
NIH-LLU Initiative for Maximizing Student DiversityR25GM060507 · NIGMS · LOMA LINDA UNIVERSITY · PI DE LEON, MARINO · 2001 to 2022
$11.3M
Maternal Hypoxia and Programming of Fetal HeartR01HL083966 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 2007 to 2011
$1.8M
Steroid Hormones and Uterine Vascular Adaptation to PregnancyR01HL089012 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 2008 to 2012
$1.8M
Uterine Vascular Adaptation to PregnancyR01HL057787 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 1998 to 2005
$1.6M
Prenatal Cocaine Exposure and Cardiac ProgrammingR01HL082779 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 2006 to 2009
$1.6M
Cocaine and Apoptosis in the Developing HeartR01HL067745 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 2001 to 2004
$820k
NHLBI NIH HHS HL57787NHLBI NIH HHS HL67745NHLBI NIH HHS HL82779NHLBI NIH HHS HL83966NHLBI NIH HHS HL89012NHLBI NIH HHS R01 HL057787NHLBI NIH HHS R01 HL067745NHLBI NIH HHS R01 HL082779NHLBI NIH HHS R01 HL083966NHLBI NIH HHS R01 HL089012NICHD NIH HHS HD31226NICHD NIH HHS P01 HD031226NIGMS NIH HHS 5R25GM060507NIGMS NIH HHS R25 GM060507
6 · The paper itself

Abstract

Fetal hearts show a remarkable ability to develop under hypoxic conditions. The metabolic flexibility of fetal hearts allows sustained development under low oxygen conditions. In fact, hypoxia is critical for proper myocardial formation. Particularly, hypoxia inducible factor 1 (HIF-1) and vascular endothelial growth factor play central roles in hypoxia-dependent signaling in fetal heart formation, impacting embryonic outflow track remodeling and coronary vessel growth. Although HIF is not the only gene involved in adaptation to hypoxia, its role places it as a central figure in orchestrating events needed for adaptation to hypoxic stress. Although "normal" hypoxia (lower oxygen tension in the fetus as compared with the adult) is essential in heart formation, further abnormal hypoxia in utero adversely affects cardiogenesis. Prenatal hypoxia alters myocardial structure and causes a decline in cardiac performance. Not only are the effects of hypoxia apparent during the perinatal period, but prolonged hypoxia in utero also causes fetal programming of abnormality in the heart's development. The altered expression pattern of cardioprotective genes such as protein kinase c epsilon, heat shock protein 70, and endothelial nitric oxide synthase, likely predispose the developing heart to increased vulnerability to ischemia and reperfusion injury later in life. The events underlying the long-term changes in gene expression are not clear, but likely involve variation in epigenetic regulation.

Indexed as

Fetal DevelopmentFetal HypoxiaCoronary VesselsEpigenomicsFetal HeartFetusGene ExpressionHeartHSP70 Heat-Shock ProteinsHumansHypoxia-Inducible Factor 1Myocardial IschemiaMyocardiumNitric Oxide Synthase Type IIIOrganogenesisOxygenHSP70 Heat-Shock ProteinsHypoxia-Inducible Factor 1Nitric Oxide Synthase Type IIIOxygenProtein Kinase C-epsilonVascular Endothelial Growth Factor A

Identifiers

PMID20712587
PMCPMC3075953
OpenAlexW1997412397

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.