Evidence map›Paper›PMID 33808635›Full record

ArticleNutrients2021

Role of HO-1 against Saturated Fatty Acid-Induced Oxidative Stress in Hepatocytes.

Noriyoshi Ogino, Koichiro Miyagawa, Kenjiro Nagaoka, Yuki Matsuura-Harada, Shihona Ogino, Masashi Kusanaga, Shinji Oe, Yuichi Honma, Masaru Harada, Masamitsu Eitoku and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 10 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

12 authors at 4 institutions in 1 country.

Noriyoshi OginoDepartment of Environmental Medicine, Kochi Medical School, Kohasu, Oko-cho, Nankoku City, Kochi 783-8505, Japan.ORCID 0000-0002-1877-7577
Koichiro MiyagawaThird Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Iseigaoka 1-1, Yahatanishi-ku, Kitakyushu 807-8555, Japan.
Kenjiro NagaokaLaboratory of Hygienic Chemistry, College of Pharmaceutical Sciences, Matsuyama University, Matsuyama, Ehime 790-8578, Japan.
Yuki Matsuura-HaradaDepartment of Biofunction Imaging Analysis, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University,1-1-1 Tsushima naka, Kita-ku, Okayama 7008530, Japan.
Shihona OginoDepartment of Environmental Medicine, Kochi Medical School, Kohasu, Oko-cho, Nankoku City, Kochi 783-8505, Japan.
Masashi KusanagaThird Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Iseigaoka 1-1, Yahatanishi-ku, Kitakyushu 807-8555, Japan.ORCID 0000-0001-8935-6203
Shinji OeThird Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Iseigaoka 1-1, Yahatanishi-ku, Kitakyushu 807-8555, Japan.
Yuichi HonmaThird Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Iseigaoka 1-1, Yahatanishi-ku, Kitakyushu 807-8555, Japan.
Masaru HaradaThird Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Iseigaoka 1-1, Yahatanishi-ku, Kitakyushu 807-8555, Japan.
Masamitsu EitokuDepartment of Environmental Medicine, Kochi Medical School, Kohasu, Oko-cho, Nankoku City, Kochi 783-8505, Japan.
Narufumi SuganumaDepartment of Environmental Medicine, Kochi Medical School, Kohasu, Oko-cho, Nankoku City, Kochi 783-8505, Japan.
Keiki OginoDepartment of Environmental Medicine, Kochi Medical School, Kohasu, Oko-cho, Nankoku City, Kochi 783-8505, Japan.
University of Occupational and Environmental Health Japan · JPKōchi University · JPMatsuyama University · JPOkayama University · JP

Funding

Japan Society for the Promotion of Science 17K15977Japan Society for the Promotion of Science 18H03039Japan Society for the Promotion of Science 20K17067
6 · The paper itself

Abstract

Increased circulating levels of free fatty acids, especially saturated ones, are involved in disease progression in the non-alcoholic fatty liver. Although the mechanism of saturated fatty acid-induced toxicity in the liver is not fully understood, oxidative stress may be deeply involved. We examined the effect of increased palmitic acid, the most common saturated fatty acid in the blood, on the liver of BALB/c mice via tail vein injection with palmitate. After 24 h, among several anti-oxidative stress response genes, only heme oxygenase-1 (HO-1) was significantly upregulated in palmitate-injected mice compared with that in vehicle-injected mice. Elevation of HO-1 mRNA was also observed in the fatty liver of high-fat-diet-fed mice. To further investigate the role of HO-1 on palmitic acid-induced oxidative stress, in vitro experiments were performed to expose palmitate to HepG2 cells. SiRNA-mediated knockdown of HO-1 significantly increased the oxidative stress induced by palmitate, whereas pre-treatment with SnCl

Indexed as

AnimalsDiet, High-FatEndoplasmic Reticulum StressFatty AcidsGene ExpressionHeme Oxygenase-1HepatocytesHep G2 CellsHumansLiverMaleMiceMice, Inbred BALB CMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseOxidative StressFatty AcidsHeme Oxygenase-1Palmitic AcidReactive Oxygen SpeciesRNA, MessengerRNA, Small Interferingfatty liverhem oxygenase-1lipotoxicityoxidative stresspalmitic acid

Identifiers

PMID33808635
PMCPMC8003531
OpenAlexW3135999963

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.