Evidence map›Paper›PMID 32057709›Full record

ArticleRedox biology2020

Tsg101 positively regulates P62-Keap1-Nrf2 pathway to protect hearts against oxidative damage.

Shan Deng, Kobina Essandoh, Xiaohong Wang, Yutian Li, Wei Huang, Jing Chen, Jiangtong Peng, Ding-Sheng Jiang, Xingjiang Mu, Chenran Wang and 6 more

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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
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  8. The role of ferroptosis in cardio-oncology.Archives of toxicology · 2024
    Review
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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

16 authors at 6 institutions in 3 countries.

Shan DengDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430022, China; Department of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA; Clinical Center for Human Genomic Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430022, China.
Kobina EssandohDepartment of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Xiaohong WangDepartment of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Yutian LiDepartment of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Wei HuangDepartment of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Jing ChenDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
Jiangtong PengDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430022, China; Clinical Center for Human Genomic Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430022, China.
Ding-Sheng JiangDivision of Cardiothoracic and Vascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Xingjiang MuDepartment of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Chenran WangDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Tianqing PengCritical Illness Research, Lawson Health Research Institute, Ontario, Canada.
Jun-Lin GuanDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Yigang WangDepartment of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.
Anil JeggaDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229, USA.
Kai HuangDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430022, China; Clinical Center for Human Genomic Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430022, China.
Guo-Chang FanDepartment of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA. Electronic address: fangg@ucmail.uc.edu.
University of Cincinnati Medical Center · USUnion Hospital · CNCincinnati Children's Hospital Medical Center · USLawson Health Research Institute · CATongji Hospital · CNUniversity of Cincinnati · US

Funding

Regulation of Lipid Catabolism by Autophagy in Neural Stem Cell of Tuberous Sclerosis ComplexR01NS103981 · NINDS · UNIVERSITY OF CINCINNATI · PI WANG, CHENRAN · 2018 to 2022
$1.8M
Tsg101 and endosomes in cardiac surgery-induced injuryR01GM126061 · NIGMS · UNIVERSITY OF CINCINNATI · PI FAN, GUO-CHANG · 2018 to 2021
$1.2M
Roles of Sectm1a in macrophages and cardiac function during sepsisR01GM132149 · NIGMS · UNIVERSITY OF CINCINNATI · PI FAN, GUO-CHANG · 2019 to 2022
$1.2M
NIGMS NIH HHS R01 GM126061NIGMS NIH HHS R01 GM132149NINDS NIH HHS R01 NS103981
6 · The paper itself

Abstract

Currently, most antioxidants do not show any favorable clinical outcomes in reducing myocardial ischemia-reperfusion (I/R) injury, suggesting an urgent need for exploring a new regulator of redox homeostasis in I/R hearts. Here, using heart-specific transgenic (TG) and knockdown (KD) mouse models, tumor susceptibility gene 101 (Tsg101) is defined as a novel cardiac-protector against I/R-triggered oxidative stress. RNA sequencing and bioinformatics data surprisingly reveal that most upregulated genes in Tsg101-TG hearts are transcribed by Nrf2. Accordingly, pharmacological inhibition of Nrf2 offsets Tsg101-elicited cardio-protection. Mechanistically, Tsg101 interacts with SQSTM1/p62 through its PRR domain, and promotes p62 aggregation, leading to recruitment of Keap1 for degradation by autophagosomes and release of Nrf2 to the nucleus. Furthermore, knockout of p62 abrogates Tsg101-induced cardio-protective effects during I/R. Hence, our findings uncover a previously unrecognized role of Tsg101 in the regulation of p62/Keap1/Nrf2 signaling cascades and provide a new strategy for the treatment of ischemic heart disease.

Indexed as

AutophagyNF-E2-Related Factor 2AnimalsDNA-Binding ProteinsEndosomal Sorting Complexes Required for TransportKelch-Like ECH-Associated Protein 1MiceOxidative StressSequestosome-1 ProteinTranscription FactorsTsg101 ProteinDNA-Binding ProteinsEndosomal Sorting Complexes Required for TransportKeap1 protein, mouseKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Sequestosome-1 ProteinTranscription FactorsTsg101 ProteinCardiac autophagyMyocardial ischemia-reperfusionNrf2Oxidative stressp62 aggregationTsg101

Identifiers

PMID32057709
PMCPMC7264471
OpenAlexW3005381132

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.