Central role for GSK3β in the pathogenesis of arrhythmogenic cardiomyopathy
Open accessAbstract
Arrhythmogenic cardiomyopathy (ACM) is characterized by redistribution of junctional proteins, arrhythmias, and progressive myocardial injury. We previously reported that SB216763 (SB2), annotated as a GSK3β inhibitor, reverses disease phenotypes in a zebrafish model of ACM. Here, we show that SB2 prevents myocyte injury and cardiac dysfunction in vivo in two murine models of ACM at baseline and in response to exercise. SB2-treated mice with desmosome mutations showed improvements in ventricular ectopy and myocardial fibrosis/inflammation as compared with vehicle-treated (Veh-treated) mice. GSK3β inhibition improved left ventricle function and survival in sedentary and exercised Dsg2 mut/mut mice compared with Veh-treated Dsg2 mut/mut mice and normalized intercalated disc (ID) protein distribution in both mutant mice. GSK3β showed diffuse cytoplasmic localization in control myocytes but ID redistribution in ACM mice. Identical GSK3β redistribution is present in ACM patient myocardium but not in normal hearts or other cardiomyopathies. SB2 reduced total GSK3β protein levels but not phosphorylated Ser 9–GSK3β in ACM mice. Constitutively active GSK3β worsens ACM in mutant mice, while GSK3β shRNA silencing in ACM cardiomyocytes prevents abnormal ID protein distribution. These results highlight a central role for GSKβ in the complex phenotype of ACM and provide further evidence that pharmacologic GSKβ inhibition improves cardiomyopathies due to desmosome mutations.
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The germline Dsg2mut/mut mouse model exhibits progressive myocardial inflammation, fibrotic remodeling, and ventricular dysfunction and arrhythmias.
“This model exhibits progressive myocardial inflammation, fibrotic remodeling, and ventricular dysfunction and arrhythmias.”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [60]
The Results section on murine Dsg2 targeting reports cardiomyopathy by 8 weeks and extensive biventricular fibrosis by 16 weeks. The Results section on SB2 treatment reports reduced ventricular function and increased ventricular ectopy in Dsg2mut/mut mice. Myocardial inflammation is reported specifically in exercised mice, however, and the paper does not establish that inflammation itself is progressive. (LLM, conf=0.85)
Experimental — accuracy not yet measuredFindings from the germline Dsg2mut/mut model demonstrate that myocardial inflammation arises intrinsically due to the presence of a desmosomal mutation, rather than solely from infiltrative immune cells, supporting the concept that inflammation is a primary driver of disease progression and an emerging therapeutic target in ACM.
“findings from this model demonstrate that myocardial inflammation arises intrinsically (i.e., from cardiomyocytes) due to the presence of a desmosomal mutation, rather than solely from infiltrative immune cells, supporting the concept that inflammation is a primary driver of disease progression and an emerging therapeutic target in ACM.”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [60]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredGSK3β localization at the intercalated disc was observed in ACM hearts, in contrast to giant cell myocarditis and cardiac sarcoidosis where GSK3β localization was predominantly cytoplasmic.
“Uniquely, GSK3β localization at the intercalated disc (ID) was observed in ACM hearts. This finding was in stark contrast to other inflammatory heart diseases, such as giant cell myocarditis and cardiac sarcoidosis, where GSK3β localization was predominantly cytoplasmic [60].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [60]
The Results section reports GSK3β at myocyte intercalated discs in all 20 ACM hearts examined, but not in giant cell myocarditis or cardiac sarcoidosis. It describes diffuse cytoplasmic localization and/or punctate bodies in sarcoidosis; it does not specify that localization was predominantly cytoplasmic in giant cell myocarditis. No page number is available in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredAberrant 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 [60]
The Discussion (page unavailable) links aberrant GSK3β signaling to ACM pathogenesis. But neither that passage nor the Results passages retrieved for NFκB describe NFκB activation or link it to GSK3β, so the specific pathway attributed to this paper is unsupported. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSuppression of Wnt and overactivation of NFκB drive pro-inflammatory, adipogenic, and fibrotic gene expression programs.
“Together, the suppression of Wnt and overactivation of NFκB drive pro-inflammatory, adipogenic, and fibrotic gene expression programs [60].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [60]
The Introduction (page unavailable) reports reduced canonical Wnt signaling in arrhythmogenic cardiomyopathy, and the Results report inflammation in a mouse model. But the paper does not establish NFκB overactivation or show that the two pathways drive the claimed pro-inflammatory, adipogenic, and fibrotic gene-expression programs. The Discussion cautions that upstream signaling pathways were not extensively studied. (LLM, conf=0.84)
Experimental — accuracy not yet measured
Pharmacological inhibition of GSK3β (SB216763) prevented myocyte injury and cardiac dysfunction in two murine models of ACM at rest and in response to exercise, with improvements in ventricular ectopy and function, myocardial fibrosis and inflammation, normalization of ID proteins, and increased survival.
“Pharmacological inhibition of GSK3β (e.g., SB216763) prevented myocyte injury and cardiac dysfunction in two murine models of ACM (Dsg2mut/mut and JUP2157del2) at rest and in response to exercise, where SB216763-treated mice demonstrated improvements in ventricular ectopy and function, myocardial fibrosis and inflammation, and normalization of ID proteins, and, most importantly, increased survival”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [60]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredThe germline Dsg2mut/mut mouse model represents a more genetically relevant system for studying ACM pathogenesis because the Dsg2 mutation is germline, mirroring the pattern of inheritance observed in patients.
“The germline Dsg2mut/mut mouse model developed by Chelko SP and colleagues represents a more genetically relevant system for studying ACM pathogenesis, as the Dsg2 mutation is germline, mirroring the pattern of inheritance observed in patients [12,60].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [60]
Uniquely distinguishing features have been noted in ACM hearts, such as loss of junctional plakoglobin, Cx43, and SAP97 at the intercalated disc, in conjunction with GSK3β redistribution to the intercalated disc, demonstrating that desmosomal disruption imparts uniquely specific pathological characteristics in ACM.
“uniquely distinguishing features have been noted in ACM hearts, such as loss of junctional plakoglobin (JUP), Cx43 [73], and SAP97 [74] at the ID, in conjunction with GSK3β redistribution to the ID [60], demonstrating that desmosomal disruption imparts uniquely specific pathological characteristics in ACM.”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [60]
Dysregulation of GSK3β has been implicated in ACM pathogenesis, particularly in promotion of fibrosis and inflammation, and is effectively inhibited by SB216763 in preclinical ACM models.
“Dysregulation of GSK3β, involved in the suppression of the Wnt/β-catenin pathway, has also been implicated in ACM pathogenesis, particularly in the promotion of fibrosis and inflammation, and is effectively inhibited by SB216763 in preclinical ACM models [60,74,116,117].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [60]
In Dsg2mut/mut mice, myocardial levels of IL-1β, IFN-γ, IL-12, LIX (CXCL5), and Osteopontin (OPN) are substantially elevated.
“In Dsg2mut/mut mice, myocardial levels of IL-1β, IFN-γ, IL-12, LIX (CXCL5), and Osteopontin (OPN) are substantially elevated.”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [60]
The Results section on exercise in Dsg2mut/mut mice reports myocardial inflammation, but not levels of the named molecules (page unavailable). Searches for IL-1β, IFN-γ, IL-12, CXCL5, and osteopontin found no passage reporting that their myocardial levels were elevated. (LLM, conf=0.76)
Experimental — accuracy not yet measuredMultiple pro-inflammatory cytokines and chemokines are upregulated early in ACM pathogenesis.
“Multiple pro-inflammatory cytokines and chemokines have been shown to be upregulated early in ACM pathogenesis.”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [60]
The Results section reports focal areas of inflammation in an ACM mouse model, but does not report increased cytokine or chemokine levels. Searches of our copy for cytokines, chemokines, and inflammatory markers found no passage showing that multiple such molecules are upregulated early in ACM pathogenesis. (LLM, conf=0.75)
Experimental — accuracy not yet measuredLIX and OPN levels show a significant inverse correlation with cardiac function and a positive correlation with myocardial fibrosis in Dsg2mut/mut mice.
“Notably, LIX and OPN levels show a significant inverse correlation with cardiac function and a positive correlation with myocardial fibrosis [60]”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [60]
The Results sections report cardiac dysfunction and myocardial fibrosis in Dsg2mut/mut mice, but do not link either outcome to LIX or OPN levels. Searches for LIX, OPN, osteopontin, and correlations found no passage addressing the claimed relationships; page numbers were not available in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measured
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Self-citationNaxos Disease and Related Cardio-Cutaneous Syndromes
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The Many Faces of Arrhythmogenic Cardiomyopathy: An Overview
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- Authors
- Chelko, S. P., Asimaki, A., Andersen, P., Bedja, D., Amat-Alarcon, N., DeMazumder, D., Jasti, R., MacRae, C. A., Leber, R., Kleber, A. G., Saffitz, J. E., & Judge, D. P.
- Affiliations
- Johns Hopkins University (US)
- Beth Israel Deaconess Medical Center (US)
- Department of Medicine/Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
- Brigham and Women's Hospital (US)
- Schiller AG, Research and Development, Baar, Switzerland.
- Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA.
- Corresponding author
- Saffitz, Jeffrey E.
- Judge, Daniel P.
- ORCID
- Venue
- JCI Insight
- Published
- 2016-04-21
- Volume
- 1
- Issue
- 5
- ISSN
- 2379-3708 (ISSN-L)
- PMC
- PMC4861310
- OpenAlex
- W2341491381
- Cited by
- 180
- References
- 39
- Citations by year
- 2026: 10 · 2025: 27 · 2024: 16 · 2023: 23 · 2022: 12 · 2021: 30 · 2020: 21 · 2019: 14 · 2018: 12 · 2017: 13 · 2016: 2
- FWCI
- 11.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- JCI Insight (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- University of Miami
- Hartwell Foundation
- National Institutes of Health (R24OD017870)
- Leonard M. Miller School of Medicine
- National Heart, Lung, and Blood Institute (RC1HL100110, K99HL130662, R01HL102361)
- 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, GSK3β, SB216763, GSK-3β inhibition, desmoglein 2, ventricular ectopy, myocardial fibrosis, exercise-induced cardiomyopathy, cardiac dysfunction, zebrafish model, mouse model, cardiomyocyte injury
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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