Evidence map›Paper›PMID 36950116›Full record

ArticleiScience2023

Hepatic ZBTB22-mediated detoxification ameliorates acetaminophen-induced liver injury by inhibiting pregnane X receptor signaling.

Yingjian Chen, Tianqi Cui, Shaorong Xiao, Tianyao Li, Yadi Zhong, Kaijia Tang, Jingyi Guo, Shangyi Huang, Jiabing Chen, Jiayu Li and 4 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.2field-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

6 citing papers in PubMed, 9 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

14 authors at 1 institution in 1 country.

Yingjian ChenScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Tianqi CuiScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Shaorong XiaoSchool of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Tianyao LiScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Yadi ZhongScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Kaijia TangScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Jingyi GuoScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Shangyi HuangScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Jiabing ChenScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Jiayu LiScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Qi WangScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Jiawen HuangScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Huafeng PanScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Yong GaoScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510080, China.
Guangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overdose acetaminophen (APAP) can cause acute liver injury (ALI), but the underlying mechanism remains undetermined. This study explored the role of hepatic Zinc Finger And BTB Domain Containing 22 (ZBTB22) in defense against APAP-mediated hepatotoxicity. The results showed that hepatic ZBTB22 expression was significantly reduced in patients with ALI and mice. In mouse primary hepatocytes (MPHs), ZBTB22 deletion aggravated APAP overdose-induced ALI, whereas ZBTB22 overexpression attenuated that pathological progression. The results were further verified in ZBTB22 over-express or knockout mice models. In parallel, hepatocyte-specific ZBTB22 knockout also enhanced ALI. Furthermore, ZBTB22 decreased pregnane X receptor (PXR) expression, and the PXR activator pregnane-16α-carbonitrile suppressed the protective effect of ZBTB22 in APAP-induced ZBTB22-overexpressing mice. Collectively, our findings highlight the protective effect of ZBTB22 against APAP-induced ALI and unravel PXR signaling as the potential mechanism. Strategies to increase hepatic ZBTB22 expression represent a promising therapeutic approach for APAP overdose-induced ALI.

Indexed as

Molecular physiologyPharmacology

Identifiers

PMID36950116
PMCPMC10025966
OpenAlexW4322771712

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.