Evidence map›Paper›PMID 31302374›Full record

ArticleThe Journal of nutritional biochemistry2019

Astaxanthin attenuates the increase in mitochondrial respiration during the activation of hepatic stellate cells.

Minkyung Bae, Yoojin Lee, Young-Ki Park, Dong-Guk Shin, Pujan Joshi, Seung-Hyun Hong, Nathan Alder, Sung I Koo, Ji-Young Lee

Open access · greenAbstract read
In one paragraph

Article in The Journal of nutritional biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 38 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

9 authors at 1 institution in 1 country.

Minkyung BaeDepartment of Nutritional Sciences, University of Connecticut, Storrs, CT, USA.
Yoojin LeeDepartment of Nutritional Sciences, University of Connecticut, Storrs, CT, USA.
Young-Ki ParkDepartment of Nutritional Sciences, University of Connecticut, Storrs, CT, USA.
Dong-Guk ShinDepartment of Computer Science and Engineering, Molecular and Cell Biology, University of Connecticut, Storrs, CT, USA.
Pujan JoshiDepartment of Computer Science and Engineering, Molecular and Cell Biology, University of Connecticut, Storrs, CT, USA.
Seung-Hyun HongDepartment of Computer Science and Engineering, Molecular and Cell Biology, University of Connecticut, Storrs, CT, USA.
Nathan AlderDepartment of Molecular and Cell Biology, University of Connecticut, Storrs, CT, USA.
Sung I KooDepartment of Nutritional Sciences, University of Connecticut, Storrs, CT, USA.
Ji-Young LeeDepartment of Nutritional Sciences, University of Connecticut, Storrs, CT, USA. Electronic address: ji-young.lee@uconn.edu.
University of Connecticut · US

Funding

Nutritional Transcriptomics Approach for the Role of Astaxanthin in Liver FibrosisR01DK108254 · NIDDK · UNIVERSITY OF CONNECTICUT STORRS · PI LEE, JI-YOUNG · 2015 to 2018
$1.5M
NIDDK NIH HHS R01 DK108254
6 · The paper itself

Abstract

Upon liver injury, quiescent hepatic stellate cells (qHSCs) transdifferentiate to myofibroblast-like activated HSCs (aHSCs), which are primarily responsible for the accumulation of extracellular matrix proteins during the development of liver fibrosis. Therefore, aHSCs may exhibit different energy metabolism from that of qHSCs to meet their high energy demand. We previously demonstrated that astaxanthin (ASTX), a xanthophyll carotenoid, prevents the activation of HSCs. The objective of this study was to determine if ASTX can exert its antifibrogenic effect by attenuating any changes in energy metabolism during HSC activation. To characterize the energy metabolism of qHSCs and aHSCs, mouse primary HSCs were cultured on uncoated plastic dishes for 7 days for spontaneous activation in the presence or absence of 25 μM ASTX. qHSCs (1 day after isolation) and aHSCs treated with or without ASTX for 7 days were used to determine parameters related to mitochondrial respiration using a Seahorse XFe24 Extracellular Flux analyzer. aHSCs had significantly higher basal respiration, maximal respiration, ATP production, spare respiratory capacity and proton leak than those of qHSCs. However, ASTX prevented most of the changes occurring during HSC activation and improved mitochondrial cristae structure with decreased cristae junction width, lumen width and the area in primary mouse aHSCs. Furthermore, qHSCs isolated from ASTX-fed mice had lower mitochondrial respiration and glycolysis than control qHSCs. Our findings suggest that ASTX may exert its antifibrogenic effect by attenuating the changes in energy metabolism during HSC activation.

Indexed as

AnimalsCells, CulturedCell TransdifferentiationDNA, MitochondrialEnergy MetabolismGene Expression RegulationGlycolysisHepatic Stellate CellsHumansMice, Inbred C57BLMitochondria, LiverTransforming Growth Factor beta1XanthophyllsastaxanthineDNA, MitochondrialTransforming Growth Factor beta1XanthophyllsAstaxanthinEnergy metabolismFibrogenesisHepatic stellate cellMitochondrial respiration

Identifiers

PMID31302374
PMCPMC6707861
OpenAlexW2949184819

What OpenQuestion holds

Textmetadata
LicenceTDM
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.