Evidence map›Paper›PMID 18346532›Full record

ReviewSeminars in perinatology2008

The role of nitric oxide in intestinal epithelial injury and restitution in neonatal necrotizing enterocolitis.

Nikunj K Chokshi, Yigit S Guner, Catherine J Hunter, Jeffrey S Upperman, Anatoly Grishin, Henri R Ford

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in perinatology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Supplementary parenteral arginine corrects hypoargininaemia and rebalances plasma amino acid profiles in very preterm infants receiving parenteral nutrition: A prospective study.Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition · 2026
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  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Update on the Pathogenesis of the Hirschsprung-Associated Enterocolitis.International journal of molecular sciences · 2023
    Review
  13. Review
  14. A Novel ProbioticMicrobiology spectrum · 2022
    Article
  15. Article
  16. Review
  17. Article
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  20. Review
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.

Nikunj K ChokshiDepartment of Pediatric Surgery, Childrens Hospital Los Angeles, Los Angeles, CA 90027, USA.
Yigit S Guner
Catherine J Hunter
Jeffrey S Upperman
Anatoly Grishin
Henri R Ford
University of Southern California · USChildren's Hospital of Los Angeles · US

Funding

Pathogenesis of Experimental Necrotizing EnterocolitisR01AI049473 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FORD, HENRI R · 2002 to 2006
$1.7M
NIAID NIH HHS R01 AI049473
6 · The paper itself

Abstract

Necrotizing enterocolitis (NEC) is the most common life-threatening gastrointestinal disease encountered in the premature infant. Although the inciting events leading to NEC remain elusive, various risk factors, including prematurity, hypoxemia, formula feeding, and intestinal ischemia, have been implicated in the pathogenesis of NEC. Data from our laboratory and others suggest that NEC evolves from disruption of the intestinal epithelial barrier, as a result of a combination of local and systemic insults. We postulate that nitric oxide (NO), an important second messenger and inflammatory mediator, plays a key role in intestinal barrier failure seen in NEC. Nitric oxide and its reactive nitrogen derivative, peroxynitrite, may affect gut barrier permeability by inducing enterocyte apoptosis (programmed cell death) and necrosis, or by altering tight junctions or gap junctions that normally play a key role in maintaining epithelial monolayer integrity. Intrinsic mechanisms that serve to restore monolayer integrity following epithelial injury include enterocyte proliferation, epithelial restitution via enterocyte migration, and re-establishment of cell contacts. This review focuses on the biology of NO and the mechanisms by which it promotes epithelial injury while concurrently disrupting the intrinsic repair mechanisms.

Indexed as

ApoptosisEnterocolitis, NecrotizingEnterocytesHumansInfant, NewbornInfant, PrematureIntestinal MucosaNitric OxidePermeabilityRisk FactorsNitric Oxide

Identifiers

PMID18346532
PMCPMC2390779
OpenAlexW2113663795

What OpenQuestion 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 OpenQuestion graph.