Evidence map›Paper›PMID 9811886›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Impaired liver regeneration in inducible nitric oxide synthasedeficient mice.

R M Rai, F Y Lee, A Rosen, S Q Yang, H Z Lin, A Koteish, F Y Liew, C Zaragoza, C Lowenstein, A M Diehl

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
10.3field-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

60 citing papers in PubMed, 246 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Nitric Oxide: Physiological Functions, Delivery, and Biomedical Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  6. Biomechanics in liver regeneration after partial hepatectomy.Frontiers in bioengineering and biotechnology · 2023
    Review
  7. Review
  8. From Cell Death to Regeneration: Rebuilding After Injury.Frontiers in cell and developmental biology · 2021
    Review
  9. Liver Regeneration after Hepatectomy and Partial Liver Transplantation.International journal of molecular sciences · 2020
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. 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

10 authors at 4 institutions in 2 countries.

R M RaiDepartment of Medicine, The Johns Hopkins University, Baltimore, MD 21205, USA.
F Y Lee
A Rosen
S Q Yang
H Z Lin
A Koteish
F Y Liew
C Zaragoza
C Lowenstein
A M Diehl
Johns Hopkins University · USGood Samaritan Hospital · USGood Samaritan Medical Center · USUniversity of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms that permit adult tissues to regenerate when injured are not well understood. Initiation of liver regeneration requires the injury-related cytokines, tumor necrosis factor (TNF) alpha and interleukin (IL) 6, and involves the activation of cytokine-regulated transcription factors such as NF-kappabeta and STAT3. During regeneration, TNFalpha and IL-6 promote hepatocyte viability, as well as proliferation, because interventions that inhibit either cytokine not only block hepatocyte DNA synthesis, but also increase liver cell death. These observations suggest that the cytokines induce hepatoprotective factors in the regenerating liver. Given evidence that nitric oxide can prevent TNF-mediated activation of the pro-apoptotic protease caspase 3 and protect hepatocytes from cytokine-mediated death, cytokine-inducible nitric oxide synthase (iNOS) may be an important hepatoprotective factor in the regenerating liver. In support of this hypothesis we report that the hepatocyte proliferative response to partial liver resection is severely inhibited in transgenic mice with targeted disruption of the iNOS gene. Instead, partial hepatectomy is followed by increased caspase 3 activity, hepatocyte death, and liver failure, despite preserved induction of TNFalpha, IL-6, NF-kappabeta, and STAT3. These results suggest that during successful tissue regeneration, injury-related cytokines induce factors, such as iNOS and its product, NO, that protect surviving cells from cytokine-mediated death.

Indexed as

Liver RegenerationAnimalsCytokinesMiceMice, KnockoutNitric Oxide SynthaseNitric Oxide Synthase Type IICytokinesNitric Oxide SynthaseNitric Oxide Synthase Type IINos2 protein, mouse

Identifiers

PMID9811886
PMCPMC24912
OpenAlexW2048599809

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.