Evidence map›Paper›PMID 31089410›Full record

ArticleOxidative medicine and cellular longevity2019

Higd1a Protects Cells from Lipotoxicity under High-Fat Exposure.

Tong Li, Wen-Jing Xian, Yang Gao, Shuai Jiang, Qi-Hong Yu, Qi-Chang Zheng, Yong Zhang

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

14 citing papers in PubMed, 19 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

7 authors at 1 institution in 1 country.

Tong LiDepartment of Hepatobiliary Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.ORCID 0000-0002-4283-0091
Wen-Jing XianDepartment of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.ORCID 0000-0003-2113-5708
Yang GaoDepartment of Hepatobiliary Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.ORCID 0000-0001-5796-8889
Shuai JiangDepartment of Hepatobiliary Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.ORCID 0000-0002-1190-6188
Qi-Hong YuDepartment of Hepatobiliary Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.ORCID 0000-0001-7364-5633
Qi-Chang ZhengDepartment of Hepatobiliary Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.ORCID 0000-0002-4198-9578
Yong ZhangDepartment of Hepatobiliary Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.ORCID 0000-0001-8034-2446
Union Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia-inducible gene domain family member 1A (Higd1a) has recently been reported to protect cells from hypoxia by helping to maintain normal mitochondrial function. The potential induction of Higd1a under high-fat exposure and whether it could protect cells from oxidative stress attracted our attention. Initially, 0.4 mM oleic acid and 0.2 mM palmitate were added to the growth media of HepG2 and LO2 cells for 72 hours. We discovered increased Higd1a expression, and knocking down Higd1a impaired mitochondrial transmembrane potential and induced cell apoptosis. We then identified that elevated reactive oxygen species (ROS) is responsible for increased Higd1a expression. Furthermore, we found that ROS promoted Higd1a expression by upregulating HIF-1a and PGC-1a expressions, and these two proteins could exert synergistic effects in inducing Higd1a expression. Taken together, these data suggest that Higd1a plays positive roles in protecting cells from oxidative stress, and ROS could induce Higd1a expression by upregulating PGC-1a and HIF-1a expressions.

Indexed as

CytoprotectionDiet, High-FatAnimalsApoptosis Regulatory ProteinsHep G2 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitIntracellular Signaling Peptides and ProteinsLipidsMembrane Potential, MitochondrialMice, Inbred C57BLMitochondrial ProteinsNeoplasm ProteinsNon-alcoholic Fatty Liver DiseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaReactive Oxygen SpeciesApoptosis Regulatory ProteinsHIGD1A protein, humanHigd1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitIntracellular Signaling Peptides and ProteinsLipidsMitochondrial ProteinsNeoplasm ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaReactive Oxygen Species

Identifiers

PMID31089410
PMCPMC6476072
OpenAlexW2939139417

What OpenQuestion holds

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LicenceCC BY
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.