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Study · Animal study (in vivo) · mouse · 2026

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Kynurenic acid mediates epicardial fat-induced lymphatic metabolic dysfunction in atrial fibrillation.

Takahashi M, Abe I, Yoshida N, Katoh D, Fujita D, Goto S, Yamasaki H, Ko T, Jiang Y, He Y, Ito S, Harada T and 13 more

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Takano M, Sato H, Kondo H, Fukui A, Teshima Y, Sako H, Ohta K, Miyamoto S, Yamauchi T, Nomura S, Takeda N, Komuro I, Takahashi N

Nature communications19 May 2026

PMID42156758 (opens in a new tab)PMCIDPMC13381822 (opens in a new tab)DOI10.1038/s41467-026-72974-9 (opens in a new tab)PepBankPUB-42156758
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Summary

Atrial fibrillation represents a prevalent cardiac arrhythmia whose pathogenic mechanisms remain incompletely understood. Here, we identify impaired atrial lymphangiogenesis as a critical determinant in atrial fibrillation pathogenesis. Analysis of human left atrial appendage specimens reveals decreased lymphatic vessel density in atrial fibrillation patients compared to those in sinus rhythm. Mechanistically, we demonstrate that epicardial adipose tissues from atrial fibrillation patients secrete kynurenic acid, which acts via GPR35 to disrupt lymphatic endothelial cell metabolism and mitochondrial homeostasis, ultimately promoting endothelial-to-mesenchymal transition. Using an organotypic culture system, we show that epicardial adipose tissue -derived factors directly impair lymphatic vessel formation. In vivo studies utilizing angiotensin II-induced and high-fat diet male mouse models confirm the critical role of lymphatic dysfunction in atrial fibrillation susceptibility. Therapeutic interventions promoting lymphangiogenesis, either through VEGFC administration or weight loss intervention by LY3437943 (the novel triple GIP, GLP-1, and glucagon receptor agonist), significantly attenuate atrial fibrillation inducibility. These findings establish lymphatic dysfunction as a novel pathogenic mechanism in atrial fibrillation and highlight lymphatic vessel formation as a promising therapeutic target.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

1 result from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In male mouse models of atrial fibrillation, weight loss with LY3437943 significantly attenuated atrial fibrillation inducibility.

    In plain wordsIn mice, weight loss with the triple agonist LY3437943 made atrial fibrillation less easy to trigger.

    Peptide
    Retatrutide
    Outcome
    DecreaseAtrial fibrillation inducibility
    Study

    mousen: not reported in source

    Angiotensin II-induced and high-fat diet male mouse models of atrial fibrillation
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Therapeutic interventions promoting lymphangiogenesis, either through VEGFC administration or weight loss intervention by LY3437943 (the novel triple GIP, GLP-1, and glucagon receptor agonist), significantly attenuate atrial fibrillation inducibility.
    1 context sentence
    Summary · context
    In vivo studies utilizing angiotensin II-induced and high-fat diet male mouse models confirm the critical role of lymphatic dysfunction in atrial fibrillation susceptibility.

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Version history

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  1. Version 2Current

    10 Oct 2026, 10:21 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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