Evidence map›Paper›PMID 42675474›Full record

ArticleJournal of biomedical science2026

Glucose-dependent insulinotropic polypeptide receptor agonism improves heart failure with antifibrosis through Akt-dependent nitric oxide signaling.

Ting-Wei Lee, Ting-I Lee, Satoshi Higa, Yu-Hsun Kao, Yi-Jen Chen

Abstract read
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In one paragraph

Article in Journal of biomedical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

5 authors.

Ting-Wei LeeDivision of Endocrinology and Metabolism, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, 11031, Taiwan.
Ting-I LeeDivision of Endocrinology and Metabolism, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, 11031, Taiwan.
Satoshi HigaCardiac Electrophysiology and Pacing Laboratory, Division of Cardiovascular Medicine, Makiminato Central Hospital, Makiminato, Urasoe, Okinawa, 901-2131, Japan.
Yu-Hsun KaoGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, No.250, Wuxing Street, Taipei, 11031, Taiwan. yuhsunkao@gmail.com.ORCID https://orcid.org/0000-0001-8687-5091
Yi-Jen ChenGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, No.250, Wuxing Street, Taipei, 11031, Taiwan. yjchen@tmu.edu.tw.

Funding

National Science and Technology Council, R.O.C. NSTC 114-2314-B-038-059the Foundation for the Development of Internal Medicine in Okinawa, Japan 07-02-005 and 07-02-006Wan Fang Hospital 111-wf-f-8
6 · The paper itself

Abstract

backgroundCardiac fibrosis is a pathological remodeling process that contributes to the development and progression of heart failure. Although glucose-dependent insulinotropic polypeptide (GIP) may exert antifibrotic effects, how GIP receptor activation regulates cardiac fibrogenesis and modulates cardiac function in heart failure remains unclear. This study investigated whether GIP receptor agonism suppresses cardiac fibroblast activity and improves heart failure and explored the underlying mechanisms by using cellular and animal models.

methodsHuman cardiac fibroblasts were treated with [D-Ala

resultsCompared with control cells, DA-GIP (300 nM)-treated cardiac fibroblasts exhibited a significantly lower migratory activity and reduced expression levels of pro-collagen IA1, pro-collagen III, and transforming growth factor-β1 proteins. Additionally, DA-GIP increased nitric oxide (NO) production and promoted endothelial NO synthase (eNOS) and protein kinase B (Akt) activation in cardiac fibroblasts. Notably, Akt inhibition blocked DA-GIP-induced eNOS activation, and treatment with N

conclusionsDA-GIP suppresses cardiac fibroblast activity through Akt-dependent eNOS activation and subsequent NO production, thereby improving cardiac remodeling and function in experimental heart failure.

Indexed as

Heart FailureNitric OxideProto-Oncogene Proteins c-aktReceptors, Gastrointestinal HormoneSignal TransductionAnimalsFibroblastsFibrosisHumansMaleRatsRats, Sprague-Dawleygastric inhibitory polypeptide receptorNitric OxideProto-Oncogene Proteins c-aktReceptors, Gastrointestinal HormoneAktFibroblastFibrosisGlucose-dependent insulinotropic polypeptideHeart failureNitric oxide

Identifiers

PMID42675474
PMCPMC13531856

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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.