Evidence map›Paper›PMID 41848035›Full record

ArticleJournal of the American Heart Association2026

Dimethyl Fumarate Reverses β-Adrenoceptor-Mediated Myocardial Fibrosis in Mice by Inhibiting Yes-Associated Protein-Regulated Expression of Intermediate-Conductance Ca

Lin-Hong Wu, Ru-Yue Bai, Jia-Yi Chen, Zheng-Da Pang, Xia-Xia Hai, Meng-Zhuan Han, Yi-Yi Yang, Yan Wang, Yi Zhang, Jie Zhang and 3 more

Abstract read
In one paragraph

Article in Journal of the American Heart Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Lin-Hong WuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.ORCID 0009-0008-3815-5338
Ru-Yue BaiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.
Jia-Yi ChenSchool of Pharmacy Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.
Zheng-Da PangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.
Xia-Xia HaiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.
Meng-Zhuan HanDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.
Yi-Yi YangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.
Yan WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.
Yi ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.ORCID 0000-0003-3795-4812
Jie ZhangSchool of Pharmacy Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.ORCID 0000-0003-2727-8806
Gang SheDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.ORCID 0000-0001-9700-0880
Xiao-Jun DuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.ORCID 0000-0001-5213-3911
Xiu-Ling DengDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences Xi'an Jiaotong University Health Science Center Xi'an Shaanxi China.ORCID 0000-0003-3908-6086

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial fibrosis is a pivotal pathological component of the failing heart where the sympatho-β-adrenergic receptor (β-AR) signaling is augmented. Intermediate-conductance Ca

methodsWe used 2 mouse models of established cardiac fibrosis induced by administration of isoproterenol (30 mg/kg per d SC) for 1 week with animals studied 4 weeks afterwards, or transgenic overexpression of β

resultsMice subjected to repeated isoproterenol injections developed myocardial inflammation and fibrosis with irreversible cardiac dysfunction. These phenotypes seen in both models were reversed by DMF treatment in vivo. Mechanistically, in both in vivo models and in cultured fibroblasts, we observed declined YAP phosphorylation and enhanced YAP nuclear localization induced by isoproterenol, changes accompanied by upregulation of K

conclusionsDMF reverses the established myocardial fibrosis following β-AR activation by inhibiting YAP nuclear localization and resultant K

Indexed as

Adaptor Proteins, Signal TransducingCardiomyopathiesCell Cycle ProteinsDimethyl FumarateFibroblastsIntermediate-Conductance Calcium-Activated Potassium ChannelsMyocardiumReceptors, Adrenergic, beta-2AnimalsCells, CulturedDisease Models, AnimalFibrosisIsoproterenolMaleMiceMice, Inbred C57BLAdaptor Proteins, Signal TransducingCell Cycle ProteinsDimethyl FumarateIntermediate-Conductance Calcium-Activated Potassium ChannelsIsoproterenolKcnn4 protein, mousePhosphoproteinsReceptors, Adrenergic, beta-2Yap1 protein, mouseYAP-Signaling Proteinsdimethyl fumarateKCa3.1 channelmyocardial fibrosisYAPβ‐adrenergic receptor

Identifiers

PMID41848035
PMCPMC13279060

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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.