Evidence map›Paper›PMID 40195661›Full record

ArticleZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences2024

Role of AMPK

Shujie Zhao, Weilun Fang, Yu Wei, Jiahui Meng, Qiao Jin, Weijin Fang

Abstract read
In one paragraph

Article in Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

6 authors.

Shujie ZhaoDepartment of Pharmacy, Third Xiangya Hospital, Central South University, Changsha 410013. zhaoshujie1999@163.com.
Weilun FangDepartment of Oncology, Third Xiangya Hospital, Central South University, Changsha 410013, China.
Yu WeiDepartment of Pharmacy, Third Xiangya Hospital, Central South University, Changsha 410013.
Jiahui MengDepartment of Pharmacy, Third Xiangya Hospital, Central South University, Changsha 410013.
Qiao JinDepartment of Oncology, Third Xiangya Hospital, Central South University, Changsha 410013, China. 352205906@qq.com.
Weijin FangDepartment of Pharmacy, Third Xiangya Hospital, Central South University, Changsha 410013.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesOver 25% of the global population is affected by metabolic dysfunction-associated fatty liver disease (MAFLD), yet its pathogenesis remains unclear. Endoplasmic reticulum stress (ERS) may be involved in the onset and progression of MAFLD. Adenosine 5'-monophosphate-activated protein kinase α2 (AMPKα2), a key regulator of hepatic energy metabolism, may influence MAFLD development via ERS modulation. This study aims to investigate the role of AMPKα2 in a high-fat diet-induced MAFLD mouse model and its regulatory effect on the inositol-requiring enzyme 1 alpha (IRE1α)-c-Jun N-terminal kinase (JNK) signaling pathway.

methodsLiver-specific AMPKα2 knockout mice on a C57BL/6 background were generated and subjected to MAFLD induction. Mice were divided into four groups: wild-type control (WT+Chow, basic diet for 12 weeks), wild-type high-fat diet (WT+HFD, high-fat diet for 12 weeks), AMPKα2 knockout control (AMPKα2 KO+Chow), and AMPKα2 knockout high-fat diet (AMPKα2 KO+HFD). Blood glucose, lipid levels, and liver function were assessed post-treatment. Liver histology was analyzed using Oil Red O, hematoxylin-eosin, Masson, and Sirius Red staining. Western blotting was used to evaluate the expression of AMPKα2, ERS markers, autophagy, apoptosis, and ferroptosis-related proteins.

resultsCompared with the WT+Chow group, the WT+HFD group showed significantly elevated blood glucose, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels (all

conclusionsHepatic AMPKα2 knockout alleviates high-fat induced MAFLD, potentially by inhibiting the IRE1α-JNK pathway and reducing autophagy.

Indexed as

AMP-Activated Protein KinasesEndoribonucleasesFatty LiverMAP Kinase Signaling SystemNon-alcoholic Fatty Liver DiseaseProtein Serine-Threonine KinasesAnimalsDiet, High-FatEndoplasmic Reticulum StressLiverMaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionAMP-Activated Protein KinasesEndoribonucleasesErn1 protein, mousePrkaa2 protein, mouseProtein Serine-Threonine Kinasesadenosine 5’-monophosphate-activated protein kinase α2autophagyendoplasmic reticulum stressferroptosismetabolic dysfunction-associated fatty liver disease

Identifiers

PMID40195661
PMCPMC11975527

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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.