Evidence map›Paper›PMID 27534694›Full record

ReviewNature reviews. Gastroenterology & hepatology2016

Necrotizing enterocolitis: new insights into pathogenesis and mechanisms.

Diego F Niño, Chhinder P Sodhi, David J Hackam

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nature reviews. Gastroenterology & hepatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 333 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
333citing papers in PubMed, 5 pooled it
31.3field-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

333 citing papers in PubMed, 5 syntheses or guidelines pooled it, 595 citations in OpenAlex.

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  19. Comparing necrotizing enterocolitis risk among extremely preterm infants by use of human-milk or bovine-milk-based fortifier.Journal of perinatology : official journal of the California Perinatal Association · 2026
    Article
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273 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

3 authors at 2 institutions in 1 country.

Diego F NiñoDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, Maryland 21287, USA.
Chhinder P SodhiDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, Maryland 21287, USA.
David J HackamDivision of Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, Maryland 21287, USA.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

TLR4 Signaling in the Pathogenesis of Surgical Necrotizing EnterocolitisR01GM078238 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2006 to 2019
$3.9M
Modulation of TLR4 and TLR9 Signaling in NECR01DK083752 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2008 to 2016
$3.4M
Maternal-Fetal AHR Signaling in the Pathogenesis and Treatment of Necrotizing EnterocolitisR01DK117186 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI HACKAM, DAVID J · 2018 to 2021
$1.5M
NIDDK NIH HHS R01 DK083752NIDDK NIH HHS R01 DK117186NIGMS NIH HHS R01 GM078238
6 · The paper itself

Abstract

Necrotizing enterocolitis (NEC) is the most frequent and lethal disease of the gastrointestinal tract of preterm infants. At present, NEC is thought to develop in the premature host in the setting of bacterial colonization, often after administration of non-breast milk feeds, and disease onset is thought to be due in part to a baseline increased reactivity of the premature intestinal mucosa to microbial ligands as compared with the full-term intestinal mucosa. The increased reactivity leads to mucosal destruction and impaired mesenteric perfusion and partly reflects an increased expression of the bacterial receptor Toll-like receptor 4 (TLR4) in the premature gut, as well as other factors that predispose the intestine to a hyper-reactive state in response to colonizing microorganisms. The increased expression of TLR4 in the premature gut reflects a surprising role for this molecule in the regulation of normal intestinal development through its effects on the Notch signalling pathway. This Review will examine the current approach to the diagnosis and treatment of NEC, provide an overview of our current knowledge regarding its molecular underpinnings and highlight advances made within the past decade towards the development of specific preventive and treatment strategies for this devastating disease.

Indexed as

AnimalsBiological FactorsBiomarkersBreast FeedingDisease Models, AnimalDisease SusceptibilityEnterocolitis, NecrotizingGastrointestinal MicrobiomeHumansInfant, NewbornInfant, PrematureInfant, Premature, DiseasesProbioticsTreatment OutcomeBiological FactorsBiomarkers

Identifiers

PMID27534694
PMCPMC5124124
OpenAlexW2512327724

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.