Evidence map›Paper›PMID 25386057›Full record

ReviewWorld journal of gastroenterology2014

Hypoxia and fatty liver.

Tomohiro Suzuki, Satoko Shinjo, Takatomo Arai, Mai Kanai, Nobuhito Goda

Open access · bronzeAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

49 citing papers in PubMed, 106 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Tomohiro SuzukiTomohiro Suzuki, Satoko Shinjo, Takatomo Arai, Mai Kanai, Nobuhito Goda, Department of Life Science and Medical BioScience, Waseda University School of Advanced Science and Engineering, Tokyo 162-8480, Japan.
Satoko ShinjoTomohiro Suzuki, Satoko Shinjo, Takatomo Arai, Mai Kanai, Nobuhito Goda, Department of Life Science and Medical BioScience, Waseda University School of Advanced Science and Engineering, Tokyo 162-8480, Japan.
Takatomo AraiTomohiro Suzuki, Satoko Shinjo, Takatomo Arai, Mai Kanai, Nobuhito Goda, Department of Life Science and Medical BioScience, Waseda University School of Advanced Science and Engineering, Tokyo 162-8480, Japan.
Mai KanaiTomohiro Suzuki, Satoko Shinjo, Takatomo Arai, Mai Kanai, Nobuhito Goda, Department of Life Science and Medical BioScience, Waseda University School of Advanced Science and Engineering, Tokyo 162-8480, Japan.
Nobuhito GodaTomohiro Suzuki, Satoko Shinjo, Takatomo Arai, Mai Kanai, Nobuhito Goda, Department of Life Science and Medical BioScience, Waseda University School of Advanced Science and Engineering, Tokyo 162-8480, Japan.
Waseda University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver is a central organ that metabolizes excessive nutrients for storage in the form of glycogen and lipids and supplies energy-producing substrates to the peripheral tissues to maintain their function, even under starved conditions. These processes require a considerable amount of oxygen, which causes a steep oxygen gradient throughout the hepatic lobules. Alcohol consumption and/or excessive food intake can alter the hepatic metabolic balance drastically, which can precipitate fatty liver disease, a major cause of chronic liver diseases worldwide, ranging from simple steatosis, through steatohepatitis and hepatic fibrosis, to liver cirrhosis. Altered hepatic metabolism and tissue remodeling in fatty liver disease further disrupt hepatic oxygen homeostasis, resulting in severe liver hypoxia. As master regulators of adaptive responses to hypoxic stress, hypoxia-inducible factors (HIFs) modulate various cellular and organ functions, including erythropoiesis, angiogenesis, metabolic demand, and cell survival, by activating their target genes during fetal development and also in many disease conditions such as cancer, heart failure, and diabetes. In the past decade, it has become clear that HIFs serve as key factors in the regulation of lipid metabolism and fatty liver formation. This review discusses the molecular mechanisms by which hypoxia and HIFs regulate lipid metabolism in the development and progression of fatty liver disease.

Indexed as

Lipid MetabolismAnimalsApoptosis Regulatory ProteinsBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Fatty LiverHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitLiverObesityOxygenRepressor ProteinsRisk FactorsSignal TransductionSleep Apnea, ObstructiveApoptosis Regulatory ProteinsBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1HIF3A protein, humanHypoxia-Inducible Factor 1, alpha SubunitOxygenRepressor ProteinsFatty liver diseaseHypoxiaHypoxia-inducible factorLipid metabolismObstructive sleep apnea

Identifiers

PMID25386057
PMCPMC4223242
OpenAlexW1985396726

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.