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Cited by 65Cardiovascular Effects of ExerciseCardiac Fibrosis and RemodelingCardiac electrophysiology and arrhythmias

Inflammation shapes pathogenesis of murine arrhythmogenic cardiomyopathy

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Lubos, Nadine, van der Gaag, Svenja, Gerçek, Muhammed, Kant, Sebastian, Leube, Rudolf E., Krusche, Claudia A.·2020·Basic Research in Cardiology
DOI 10.1007/s00395-020-0803-5PMC PMC7289786
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Abstract

Arrhythmogenic cardiomyopathy (AC) is an incurable genetic disease, whose pathogenesis is poorly understood. AC is characterized by arrhythmia, fibrosis, and cardiodilation that may lead to sudden cardiac death or heart failure. To elucidate AC pathogenesis and to design possible treatment strategies of AC, multiple murine models have been established. Among them, mice carrying desmoglein 2 mutations are particularly valuable given the identification of desmoglein 2 mutations in human AC and the detection of desmoglein 2 auto-antibodies in AC patients. Using two mouse strains producing either a mutant desmoglein 2 or lacking desmoglein 2 in cardiomyocytes, we test the hypothesis that inflammation is a major component of disease pathogenesis. We show that multifocal cardiomyocyte necrosis initiates a neutrophil-dominated inflammatory response, which also involves macrophages and T cells. Increased expression of Ccl2/Ccr2, Ccl3/Ccr5, and Cxcl5/Cxcr2 mRNA reflects the observed immune cell recruitment. During the ensuing acute disease phase, Mmp12+ and Spp1+ macrophages and T cells accumulate in scars, which mature from cell- to collagen-rich. The expression of Cx3cl1/Cx3cr1, Ccl2/Ccr2, and Cxcl10/Cxcr3 dominates this disease phase. We furthermore find that during chronic disease progression macrophages and T cells persist within mature scars and are present in expanding interstitial fibrosis. Ccl12 and Cx3cl1 are predominant chemokines in this disease phase. Together, our observations provide strong evidence that specific immune cell populations and chemokine expression profiles modulate inflammatory and repair processes throughout AC progression.

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  • NFκB is activated downstream of desmosome disruption through increased mechanical stretch, ER stress, ROS, and autocrine production of cytokines.

    “NFκB is activated downstream of desmosome disruption through increased mechanical stretch, endoplasmic reticulum (ER) stress, reactive oxygen species (ROS), and the autocrine production of cytokines [78].”

    From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [78]

    The Results sections on early cardiomyopathy and scar formation report inflammatory responses and increased cytokine expression in desmoglein-2 mutant mice. They do not address whether NFκB is activated by desmosome disruption through mechanical stretch, ER stress, ROS, or autocrine cytokines. Searches for NFκB, nuclear factor kappa B, and those proposed mechanisms found no passage establishing that pathway. (LLM, conf=0.76)

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Cited by

Sorted by citations

Authors
Lubos, N., van der Gaag, S., Gerçek, M., Kant, S., Leube, R. E., & Krusche, C. A.
Affiliations
RWTH Aachen University (DE)
Corresponding author
  • Leube, Rudolf E.
  • Krusche, Claudia A.
ORCID
Venue
Basic Research in Cardiology
Publisher
Springer Science and Business Media LLC
Published
2020-06-12
Volume
115
Issue
4
Pages
42-42
ISSN
  • 0003-9217 (ISSN-L)
  • 0300-8428
  • 1435-1803
DOI
10.1007/s00395-020-0803-5
PMC
PMC7289786
OpenAlex
W3034875393
Cited by
65
References
7
Citations by year
2026: 8 · 2025: 11 · 2024: 10 · 2023: 7 · 2022: 10 · 2021: 17 · 2020: 2
FWCI
5.57
Type
journal article
Language
en
Open access
Licence
Locations
  • Basic Research in Cardiology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Informationszentrum Lebenswissenschaften (ZB MED) (submittedVersion, cc-by)
  • RWTH Publications (RWTH Aachen) (submittedVersion, other-oa)
Funders
  • Deutsche Herzstiftung
  • RWTH Aachen University
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Effects of Exercise
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords
arrhythmogenic cardiomyopathy, inflammation, desmoglein 2, myocardial necrosis, neutrophils, macrophages, T cells, chemokines, interstitial fibrosis, fractalkine, CCL12, CXCL10, CCL2/CCR2, disease progression, mouse model
MeSH terms
Animals, Arrhythmias, Cardiac, Inflammation, Mice, Mutant Strains, Mutation, Cardiomyopathies, Desmoglein 2, Mice

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