Evidence map›Paper›PMID 31505325›Full record

ArticleRedox biology2020

Peroxiredoxin 5 ameliorates obesity-induced non-alcoholic fatty liver disease through the regulation of oxidative stress and AMP-activated protein kinase signaling.

Mi Hye Kim, Jung Bae Seong, Jae-Won Huh, Yong Chul Bae, Hyun-Shik Lee, Dong-Seok Lee

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 80 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

6 authors at 2 institutions in 1 country.

Mi Hye KimSchool of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu, South Korea; School of Life Sciences & Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, South Korea.
Jung Bae SeongSchool of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu, South Korea; School of Life Sciences & Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, South Korea.
Jae-Won HuhNational Primate Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, South Korea.
Yong Chul BaeDepartment of Anatomy and Neurobiology, School of Dentistry, Kyungpook National University, Daegu, South Korea.
Hyun-Shik LeeSchool of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu, South Korea; School of Life Sciences & Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, South Korea.
Dong-Seok LeeSchool of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu, South Korea; School of Life Sciences & Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, South Korea. Electronic address: lee1@knu.ac.kr.
Kyungpook National University · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is becoming the most common chronic liver disease globally. NAFLD-which can develop into liver fibrosis, nonalcoholic steatohepatosis, cirrhosis, and hepatocellular carcinoma-is defined as an excess accumulation of fat caused by abnormal lipid metabolism and excessive reactive oxygen species (ROS) generation in hepatocytes. Recently, we reported that Peroxiredoxin 5 (Prx5) plays an essential role in regulating adipogenesis and suggested the need to further investigation on the potential curative effects of Prx5 on obesity-induced fatty liver disease. In the present study, we focused on the role of Prx5 in fatty liver disease. We found that Prx5 overexpression significantly suppressed cytosolic and mitochondrial ROS generation. Additionally, Prx5 regulated the AMP-activated protein kinase pathway and lipogenic gene (sterol regulatory element binding protein-1 and FAS) expression; it also inhibited lipid accumulation, resulting in the amelioration of free fatty acid-induced hepatic steatosis. Silence of Prx5 triggered de novo lipogenesis and abnormal lipid accumulation in HepG2 cells. Concordantly, Prx5 knockout mice exhibited a high susceptibility to obesity-induced hepatic steatosis. Liver sections of Prx5-deletion mice fed on a high-fat diet displayed Oil Red O-stained dots and small leaky shapes due to immoderate fat deposition. Collectively, our findings suggest that Prx5 functions as a protective regulator in fatty liver disease and that it may be a valuable therapeutic target for the management of obesity-related metabolic diseases.

Indexed as

AMP-Activated Protein KinasesAnimalsDiet, High-FatDisease Models, AnimalGene Knockout TechniquesHep G2 CellsHumansLipid MetabolismMaleMiceNon-alcoholic Fatty Liver DiseaseObesityOxidative StressPeroxiredoxinsSignal TransductionAMP-Activated Protein KinasesPeroxiredoxinsPRDX5 protein, humanPrdx5 protein, mouseAMPKHepatic steatosisNAFLDPeroxiredoxin 5ROSSREBP-1

Identifiers

PMID31505325
PMCPMC6736789
OpenAlexW2972167367

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.