Therapeutic Modulation of the Immune Response in Arrhythmogenic Cardiomyopathy
Open accessAbstract
Background: Inflammation is a prominent feature of arrhythmogenic cardiomyopathy (ACM), but whether it contributes to the disease phenotype is not known. Methods: To define the role of inflammation in the pathogenesis of ACM, we characterized nuclear factor-κB signaling in ACM models in vitro and in vivo and in cardiac myocytes from patient induced pluripotent stem cells. Results: Activation of nuclear factor-κB signaling, indicated by increased expression and nuclear accumulation of phospho-RelA/p65, occurred in both an in vitro model of ACM (expression of JUP 2157del2 in neonatal rat ventricular myocytes) and a robust murine model of ACM (homozygous knock-in of mutant desmoglein-2 [ Dsg2 mut/mu t ]) that recapitulates the cardiac manifestations seen in patients with ACM. Bay 11-7082, a small-molecule inhibitor of nuclear factor-κB signaling, prevented the development of ACM disease features in vitro (abnormal redistribution of intercalated disk proteins, myocyte apoptosis, release of inflammatory cytokines) and in vivo (myocardial necrosis and fibrosis, left ventricular contractile dysfunction, electrocardiographic abnormalities). Hearts of Dsg2 mut/mut mice expressed markedly increased levels of inflammatory cytokines and chemotactic molecules that were attenuated by Bay 11-7082. Salutary effects of Bay 11-7082 correlated with the extent to which production of selected cytokines had been blocked. Nuclear factor-κB signaling was also activated in cardiac myocytes derived from a patient with ACM. These cells produced and secreted abundant inflammatory cytokines under basal conditions, and this was also greatly reduced by Bay 11-7082. Conclusions: Inflammatory signaling is activated in ACM and drives key features of the disease. Targeting inflammatory pathways may be an effective new mechanism-based therapy for ACM.
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Elevated levels of circulating and myocardial inflammatory cytokines and chemokines from DGV-linked ACM subjects have been observed across disease phases and phenotypes.
“Prior works have shown elevated levels of circulating [22] and myocardial inflammatory cytokines and chemokines from DGV-linked ACM subjects [11,23] that have been observed across disease phases and phenotypes”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
The Results section on cytokine production reports elevated inflammatory cytokines and chemokines in hearts of Dsg2-mutant ACM mice; the patient-derived cells studied were cultured cardiomyocytes, not myocardial samples. The paper does not establish that myocardial elevations occur in ACM subjects across disease phases and phenotypes. The circulating-level claim is attached to a different citation. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMyocardial inflammation arises as an intrinsic consequence of the Dsg2 mutation, reflecting mutation-driven inflammatory remodeling.
“these authors demonstrated myocardial inflammation arises as an intrinsic consequence of the Dsg2 mutation [11,12], reflecting mutation-driven inflammatory remodeling.”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
The Results (‘Cytokines are produced by cardiac myocytes and infiltrating inflammatory cells in ACM’; page unavailable) show increased inflammatory mediators and infiltrating cells in Dsg2-mutant mouse hearts compared with wild-type hearts. The Discussion reports cell-autonomous inflammatory signaling in cardiac myocytes with desmosomal variants, but says it remains unclear whether infiltrating cells accumulate as a response to myocardial damage. The paper therefore supports inflammation associated with the Dsg2-mutant phenotype, but not the unqualified claim that all myocardial inflammation is an intrinsic consequence of that mutation. (LLM, conf=0.83)
Experimental — accuracy not yet measuredACM is an inflammatory disease where cardiomyocytes harboring DGVs lead to NFκB activation, propagating inflammatory cascades that lead to ACM disease onset and progression.
“ACM is increasingly recognized as an inflammatory disease where cardiomyocytes harboring DGVs lead to NFκB activation, propagating inflammatory cascades that lead to ACM disease onset and progression [11].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
The Abstract Results and Discussion report NFκB activation and inflammatory cytokine release in cardiomyocytes carrying ACM-associated desmosomal gene variants; NFκB inhibition also prevented disease features in experimental models. The Introduction says these inflammatory responses could contribute to disease onset and progression. The claim states that causal role as established for ACM generally, beyond what the paper demonstrates. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAberrant signaling pathways lead to chemokine and cytokine production, facilitating local inflammation and recruitment of inflammatory cells to the heart, further amplifying arrhythmogenesis and clinical manifestations.
“These aberrant signaling pathways (Figure 3) lead to chemokine and cytokine production, facilitating local inflammation and recruitment of inflammatory cells to the heart, further amplifying arrhythmogenesis and clinical manifestations [11,12].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
The Discussion reports that NFκB signaling in ACM cardiac myocytes induces cytokines and chemoattractants that likely recruit inflammatory cells to the heart. It also says immune signaling may drive clinical features, but explicitly notes that the results do not prove cytokines cause arrhythmias or myocardial damage; the claim presents that final causal step more firmly than the source does. Page numbers are unavailable in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIntrinsic NFκB activation is demonstrated by increased nuclear localization and elevated expression of NFκB-mediated gene transcripts, independent of exogenous inflammatory stimuli.
“This intrinsic activation is demonstrated by increased NFκB nuclear localization and elevated expression of NFκB-mediated gene transcripts, independent of exogenous inflammatory stimuli [11,12].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
The Results section on ACM patient iPSC-cardiac myocytes (page unavailable) reports nuclear accumulation of phospho-RelA/p65 and abundant cytokine production under basal conditions, without provocative stimuli. It supports intrinsic NFκB activation, but reports cytokine expression and secretion rather than elevated NFκB-mediated gene transcripts. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Increased NFκB activation, evidenced by RelA/p65 nuclear localization, is observed in iPSC-CMs from ACM patients and in in vitro and in vivo models of ACM.
“Increased NFκB activation (evidenced by RelA/p65 nuclear localization) is observed in iPSC-CMs generated from patients with ACM, as well as in in vitro and in vivo models of ACM.”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
The Results report nuclear accumulation of phospho-RelA/p65 in ACM patient iPSC-derived cardiac myocytes and in the in vitro ACM model. The in vivo Results also report increased NFκB activation in mutant mouse hearts, but document it through increased phospho-RelA/p65 in myocardial homogenates, not nuclear localization. Thus the claimed evidence for activation does not fully apply to the in vivo model. (LLM, conf=0.84)
Experimental — accuracy not yet measuredDownstream NFκB activation leads to expression of inflammatory chemokines (LIX, CCL2, CXCL10) and cytokines (IL-1β, IL-6, TNFα), which are tied to recruitment of inflammatory cells and maladaptive tissue remodeling.
“Downstream NFκB activation leads to the expression of inflammatory chemokines (e.g., LIX, CCL2, CXCL10) and cytokines (e.g., IL-1β, IL-6, TNFα), which have been tied to the recruitment of inflammatory cells and maladaptive tissue remodeling [11].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
The Results (page unavailable) report increased LIX, IL-1β and TNFα in ACM mouse hearts, with inflammatory-mediator expression generally reduced by NFκB inhibition. The Discussion (page unavailable) links LIX to neutrophil chemotaxis and fibrosis, while noting that the study does not prove cytokines cause myocardial damage. The passages found do not substantiate the cited examples CCL2, CXCL10 or IL-6. (LLM, conf=0.85)
Experimental — accuracy not yet measuredNFκB downstream functions lead to recruitment of CCR2+ monocyte-derived macrophages to the hearts of ACM subjects and subsequent remodeling of ion channels and gap junctions.
“NFκB has multiple downstream functions that lead to the recruitment of CCR2+ monocyte-derived macrophages to the hearts of ACM subjects and the subsequent remodeling of ion channels and gap junctions.”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
The Results sections report NFκB-dependent cytokine production, macrophage infiltration in ACM mouse hearts, and restoration of the gap-junction protein Cx43’s distribution after NFκB inhibition. They do not identify the infiltrating macrophages as CCR2+ or monocyte-derived, or show that their recruitment subsequently causes ion-channel and gap-junction remodeling. The Discussion presents an effect of cardiac-myocyte cytokines on ion channels as a possibility, not an established sequence. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThese collective changes lead to slowed conduction, arrhythmias, and cardiac dysfunction.
“These collective changes lead to slowed conduction, arrhythmias, and cardiac dysfunction [11,12].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
The Results section (page unavailable) reports arrhythmias and progressive deterioration of ventricular contractile function in ACM mice alongside structural and protein-distribution changes. The Discussion (page unavailable) suggests that immune signaling may contribute to these disease features, but the passages do not establish slowed conduction or that the collective changes cause all three outcomes. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe small-molecule inhibitor of NFκB, Bay 11-7082, mitigates inflammation, fibrosis, cardiac dysfunction, and arrhythmogenesis in preclinical models.
“The small-molecule inhibitor of NFκB, Bay 11-7082, has shown to mitigate inflammation, fibrosis, cardiac dysfunction, and arrhythmogenesis in preclinical models [11].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
The Results section reports that Bay 11–7082 reduced inflammatory mediators in cultured ACM myocytes and, in ACM mice, reduced fibrosis and normalized contractile function. It also reports correction of ECG abnormalities, but does not show that treatment reduced arrhythmia occurrence; that is narrower evidence than the claim that it mitigates arrhythmogenesis. (LLM, conf=0.86)
Experimental — accuracy not yet measuredGrowing evidence implicates immune-mediated inflammatory mechanisms in ACM disease onset and progression.
“growing evidence implicates immune-mediated inflammatory mechanisms in disease onset and progression [11,12].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
Inflammatory processes in ACM may represent more than just an epiphenomenon of immune cell-mediated cardiomyocyte injury.
“suggesting that inflammatory processes may represent more than just an epiphenomenon of immune cell-mediated cardiomyocyte injury.”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
Aberrant GSK3β activity in ACM is linked to deleterious activation of NFκB.
“Aberrant GSK3β activity in ACM is also linked to the deleterious activation of NFκB [11,12,60].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
The NFκB signaling axis represents a central regulator of inflammatory responses implicated in ACM, and its inhibition by Bay11-7082 attenuated ACM phenotypes in preclinical models.
“The NFκB signaling axis represents a central regulator of inflammatory responses implicated in ACM, and its inhibition by Bay11-7082 attenuated ACM phenotypes in preclinical models [11,12].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [11]
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Self-citation
- Authors
- Chelko, S. P., Asimaki, A., Lowenthal, J., Bueno-Beti, C., Bedja, D., Scalco, A., Amat-Alarcon, N., Andersen, P., Judge, D. P., Tung, L., & Saffitz, J. E.
- Affiliations
- Johns Hopkins University (US)
- St George's, University of London (GB)
- St. George’s University of London, UK (A.A., C.B.-B.).
- University of Padua (IT)
- Departments of Medicine (S.P.C., D.B., N.A.-A., P.A.), Johns Hopkins School of Medicine, Baltimore, MD.
- Medical University of South Carolina (US)
- Beth Israel Deaconess Medical Center (US)
- ORCID
- Venue
- Circulation
- Published
- 2019-10-29
- Volume
- 140
- Issue
- 18
- Pages
- 1491-1505
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- PMC
- PMC6817418
- OpenAlex
- W2974365689
- Cited by
- 192
- References
- 38
- Citations by year
- 2026: 22 · 2025: 33 · 2024: 28 · 2023: 31 · 2022: 20 · 2021: 29 · 2020: 28 · 2019: 1
- FWCI
- 14.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- St George's Online Research Archive (St George's University of London) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- British Heart Foundation (PG/18/27/33616)
- National Institutes of Health (UL1TR001079)
- National Heart, Lung, and Blood Institute (R01HL120959, R01HL102361)
- National Institute of General Medical Sciences (T32GM136577)
- National Center for Advancing Translational Sciences
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD086026)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Effects of Exercise
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Keywords
- arrhythmogenic cardiomyopathy, inflammation, BAY 11-7082, desmoglein 2, cardiomyocytes, inflammatory cytokines, myocardial fibrosis, cardiomyocyte apoptosis
- MeSH terms
- Animals, Arrhythmias, Cardiac, Inflammation, Cardiomyopathies, Myocardial Infarction, Myocardium, Cytokines, Rats, Wistar, Ventricular Dysfunction, Left, Myocytes, Cardiac, Rats, Transgenic
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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