Evidence map›Paper›PMID 37999791›Full record

ArticlePediatric surgery international2023

Potential mechanisms underlying the effect of hepatocyte growth factor on liver injury in short bowel syndrome model rats.

Koshiro Sugita, Keisuke Yano, Makoto Matsukubo, Yumiko Iwamoto, Masato Ogata, Lynne Takada, Chihiro Kedoin, Masakazu Murakami, Toshio Harumatsu, Shun Onishi and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Pediatric surgery international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

16 authors at 3 institutions in 1 country.

Koshiro Sugita *Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan.
Keisuke Yano *Department of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan.
Makoto MatsukuboDepartment of Pediatric Surgery, Kagoshima City Hospital, Kagoshima, Japan.
Yumiko IwamotoDepartment of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan.
Masato OgataDepartment of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan.
Lynne TakadaDepartment of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan.
Chihiro KedoinDepartment of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan.
Masakazu MurakamiDepartment of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan.
Toshio HarumatsuDepartment of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan.
Shun OnishiDepartment of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan.
Takafumi KawanoDepartment of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan.
Mitsuru MutoDepartment of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan.
Kotaro KumagaiDigestive and Lifestyle Diseases, Department of Human and Environmental Sciences, School of Medical and Dental Sciences, Kagoshima University Graduate, Kagoshima, Japan.
Akio IdoDigestive and Lifestyle Diseases, Department of Human and Environmental Sciences, School of Medical and Dental Sciences, Kagoshima University Graduate, Kagoshima, Japan.
Tatsuru KajiDepartment of Pediatric Surgery, Kurume University School of Medicine, Kurume, Japan.
Satoshi IeiriDepartment of Pediatric Surgery, Research Field in Medical and Health Sciences, Medical and Dental Area, Research and Education Assembly, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima City, 890-8520, Japan. sieiri@m.kufm.kagoshima-u.ac.jp.
Kagoshima University · JPKagoshima City Hospital · JPKurume University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe purpose of this study was to investigate the autophagy associated with apoptosis in hepatic damage in the short bowel syndrome rat model.

methodsSD rats underwent jugular vein catheterization for continuous total parenteral nutrition (TPN) and 90% small bowel resection. Animals were divided into two groups: TPN plus SBS (Control group) or TPN plus SBS plus intravenous administration of HGF (HGF group). On day 7, the rats were harvested, and hepatocellular injury was evaluated.

resultsIn an SBS rat model, hepatic steatosis and lobular inflammation were histologically suppressed in the HGF group (p < 0.01). The expression of tumor necrosis factor-α in the HGF group tend to be higher than that in the control group (p = 0.13). The gene expression of transforming Growth Factor-β in the HGF group was suppressed compared to the control group (p < 0.01). HGF treatment may have an antiapoptotic effect via the intrinsic pathway by caspase 9. Protein expressions of Rubicon (p = 0.03) and p62 (p < 0.01) in the HGF group were found to have increased compared to those in the control group.

conclusionThe inhibitory effect of HGF on hepatic steatosis remains unclear, and further studies focusing on the mechanisms of fat accumulation are needed.

Indexed as

Liver DiseasesShort Bowel SyndromeAnimalsDisease Models, AnimalHepatocyte Growth FactorRatsRats, Sprague-DawleyHepatocyte Growth FactorApoptosisAutophagyHepatic steatosisHepatocyte growth factorShort bowel syndrome

Identifiers

PMID37999791
OpenAlexW4388969572

What OpenQuestion holds

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Read underepoch 390

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.