Evidence map›Paper›PMID 28504722›Full record

ArticleOncogene2017

Thyroid hormone protects hepatocytes from HBx-induced carcinogenesis by enhancing mitochondrial turnover.

H-C Chi, S-L Chen, S-L Lin, C-Y Tsai, W-Y Chuang, Y-H Lin, Y-H Huang, M-M Tsai, C-T Yeh, K-H Lin

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025
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  9. Mechanism and regulation of mitophagy in liver diseases: a review.Frontiers in cell and developmental biology · 2025
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  14. Article
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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

10 authors at 4 institutions in 1 country.

H-C ChiDepartment of Biochemistry, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
S-L ChenDepartment of Life Sciences, National Central University, Jhongli, Taiwan.
S-L LinDepartment of Biochemistry, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
C-Y TsaiKidney Research Center and Department of Nephrology, Chang Gung Immunology Consortium, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
W-Y ChuangDepartment of Pathology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taoyuan, Taiwan.
Y-H LinDepartment of Biochemistry, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Y-H HuangLiver Research Center, Department of Hepato-Gastroenterology, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
M-M TsaiDepartment of Nursing, Chang Gung University of Science and Technology, Taoyuan, Taiwan.
C-T YehLiver Research Center, Department of Hepato-Gastroenterology, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
K-H LinDepartment of Biochemistry, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Chang Gung University · TWChang Gung Memorial Hospital · TWChiayi Chang Gung Memorial Hospital · TWNational Central University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infection by hepatitis B virus (HBV) accounts for 50-80% of hepatocellular carcinoma (HCC) development worldwide, in which the HBV-encoded X protein (HBx) has critical role in the induction of carcinogenesis. Several studies have shown that thyroid hormone (TH) suppresses HCC development and protects hepatocytes from HBx-induced damage, thus it is of interest to examine whether TH can protect hepatocytes from HBx-induced carcinogenesis. By treating HBx- transgenic mice with or without TH, we confirmed the protective effects of TH on HBx-induced hepatocarcinogenesis, which was achieved via reduction of reactive oxygen species (ROS) inflicted DNA damage. We further found that TH induced biogenesis of mitochondria (MITO) and autophagy of HBx-targeted MITO simultaneously, consequently leading to suppression of HBx-promoted ROS and carcinogenesis. Using microarray data analysis, this protective effect of TH was found to be mediated via activation of PTEN-induced kinase 1 (PINK1) in hepatocytes. PINK1, in turn, activated and recruited Parkin, an E3 ligase, to ubiquitinate MITO-associated HBx protein and trigger selective mitophagy. The pathological significance of the TH/PINK1 pathway in liver protection was confirmed by the concomitant decrease in expression of both TR and PINK1 in matched HCC tumor tissues and negatively correlated with aggressive progression of cancer and poor prognosis. Our data indicate that TH/PINK1/Parkin pathway has a critical role in protecting hepatocytes from HBx-induced carcinogenesis. Notably, several liver-targeting therapeutic derivatives of TH facilitating prevention or therapy of steatosis have been identified. Furthermore, our proof-of-concept experiments suggest that application of T

Indexed as

AnimalsCarcinogenesisCarcinoma, HepatocellularDNA DamageHepatocytesHep G2 CellsHumansLiver NeoplasmsLiver Neoplasms, ExperimentalMaleMiceMice, TransgenicMitochondriaProtein KinasesPTEN-Induced Putative KinaseSignal Transductionhepatitis B virus X proteinProtein KinasesPTEN-Induced Putative KinaseTrans-ActivatorsTriiodothyronineViral Regulatory and Accessory Proteins

Identifiers

PMID28504722
OpenAlexW2614893092

What OpenQuestion holds

Textmetadata
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.