Evidence map›Paper›PMID 41928256›Full record

ArticleJournal of inflammation (London, England)2026

Electroacupuncture activates the TET1/PPARα pathway to protect mitochondrial function in MASLD.

Shurui Yang, Yiwen Li, Bowen Lu, Congcong Cheng, Yayuan Wang, Li Chen

Abstract read
In one paragraph

Article in Journal of inflammation (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Shurui Yang *Acupuncture and Moxibustion Department, Hubei Provincial Hospital of Traditional Chinese Medicine, Affiliated Hospital of Hubei University of Chinese Medicine, Wuhan, China.
Yiwen Li *College of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan, China.
Bowen LuCollege of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan, China.
Congcong ChengCollege of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan, China.
Yayuan WangCollege of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan, China. 18908630916@163.com.
Li ChenCollege of Acupuncture and Orthopedics, Hubei University of Chinese Medicine, Wuhan, China. 3051@hbucm.edu.cn.

Funding

National Natural Science Foundation of China 82305401Natural Science Foundation of Hubei Province 2023AFD140Research Project of the National Renowned TCM Master (Prof. Wang Hua) Heritage Workshop/Hubei Provincial Collaborative Innovation Center of Preventive Treatment by Acupuncture and Moxibustion QZ202508
6 · The paper itself

Abstract

backgroundMetabolic associated steatotic liver disease (MASLD), characterized by mitochondrial dysfunction. It may be ameliorated by electroacupuncture (EA) through activation of the ten-eleven translocation 1 (TET1)/peroxisome proliferator-activated receptor-α (PPARα) pathway, thereby restoring mitochondrial function.

methodsC57BL/6 mice were fed L-amino acid rodent diet with 60 kcal% fat, low methionine and no added choline (CDAHFD) and high fat diet (HFD) for three weeks to induce MASLD, followed by EA treatment and daily intraperitoneal injections of a TET1 agonist or antagonist. Hepatic lipid accumulation, inflammatory cytokines, reactive oxygen species (ROS), and mitochondrial function were evaluated by biochemical assays, enzyme-linked immunosorbent assay (ELISA), flow cytometry, and transmission electron microscopy (TEM), western blotting (WB) and reverse transcription quantitative polymerase chain reaction (RT-qPCR).

resultsEA reduced hepatic total cholesterol (TC), triglycerides (TG), and free fatty acids (FFA), and decreased the size of lipid droplets. It restored mitochondrial membrane potential, ATP production, and cristae integrity, while attenuating ROS accumulation and suppressing pro-inflammatory cytokine levels. Moreover, EA upregulated TET1 expression, enhanced genomic 5-hydroxymethylcytosine (5-hmC) enrichment, and elevated PPARα expression. These effects were comparable to those of a TET1 agonist, whereas administration of a TET1 antagonist partially reversed them.

conclusionEA ameliorates MASLD by activating the TET1/PPARα pathway, thereby enhancing mitochondrial function and reducing oxidative stress and inflammation. CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

AcupunctureMASLDMitochondrial functionPPAR αTET1

Identifiers

PMID41928256
PMCPMC13170153

What Socratic 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 Socratic graph.