Evidence map›Paper›PMID 40341987›Full record

ArticleArchives of pharmacal research2025

Deficiency of β-arrestin2 ameliorates MASLD in mice by promoting the activation of TAK1/AMPK signaling.

Ting-Ting Chen, Shan Shan, Ya-Ning Chen, Meng-Qi Li, Hui-Juan Zhang, Ling Li, Ping-Ping Gao, Nan Li, Yan Huang, Xiao-Lei Li and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Archives of pharmacal research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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

12 authors.

Ting-Ting Chen *Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, Anhui, China.
Shan Shan *Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, Anhui, China.
Ya-Ning ChenInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, Anhui, China.
Meng-Qi LiInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, Anhui, China.
Hui-Juan ZhangInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, Anhui, China.
Ling LiInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, Anhui, China.
Ping-Ping GaoInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, Anhui, China.
Nan LiInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, Anhui, China.
Yan HuangInflammation and Immune Mediated Diseases Laboratory of Anhui Province, School of Pharmacy, Anhui Medical University, Hefei, 230032, Anhui, China.
Xiao-Lei LiInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, Anhui, China.
Wei WeiInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, Anhui, China. wwei@ahmu.edu.cn.
Wu-Yi SunInstitute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Anhui Medical University, Hefei, 230032, Anhui, China. sunwuyi51@aliyun.com.

Funding

National Natural Science Foundation of China 82370632Postgraduate Academic Innovation Project of Anhui Province 2023xscx057Research Fund of Anhui Institute of Translational Medicine 2022zhyx-C07Research Level Improvement Program of Anhui Medical University 2021xkjT016Research Project for Distinguished Young Scholar in Universities of Anhui Province 2023AH020033
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a liver manifestation of metabolic syndrome characterized by excessive hepatic lipid accumulation and lipid metabolism disorders. It has become the most common chronic liver disease worldwide. β-arrestin2 is a multifunctional scaffold protein that is among the most important regulatory molecules, and it exerts key roles in regulating various cellular processes, such as immune response, cellular collagen production, and inflammation. In the current study, we aimed to explore the function of β-arrestin2 in the development and progression of MASLD. Firstly, we observed that the expression of β-arrestin2 was upregulated in liver samples from patients with MASLD. Then, the western diet (WD) combined with CCl

Indexed as

AMP-Activated Protein Kinasesbeta-Arrestin 2Fatty LiverMAP Kinase Kinase KinasesAnimalsDisease Models, AnimalHumansMaleMAP Kinase Kinase Kinase 7MiceMice, Inbred C57BLMice, KnockoutSignal TransductionAMP-Activated Protein KinasesArrb2 protein, mousebeta-Arrestin 2MAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesAMPKLipid accumulationMetabolic dysfunction-associated steatotic liver diseaseTABTAK1β-arrestin2

Identifiers

PMID40341987

What OpenQuestion holds

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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.