Cardiomyocyte and stromal cell cross-talk influences the pathogenesis of arrhythmogenic cardiomyopathy: a multi-level analysis uncovers DLK1-NOTCH pathway role in fibro-adipose remodelling
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Arrhythmogenic Cardiomyopathy (ACM) is a life-threatening, genetically determined disease primarily caused by mutations in desmosomal genes, such as PKP2. Currently, there is no etiological therapy for ACM due to its complex and not fully elucidated pathogenesis. Various cardiac cell types affected by the genetic mutation, such as cardiomyocytes (CM) and cardiac mesenchymal stromal cells (cMSC), individually contribute to the ACM phenotype, driving functional abnormalities and fibro-fatty substitution, respectively. However, the relative importance of the CM and cMSC alterations, as well as their reciprocal influence in disease progression remain poorly understood. We hypothesised that ACM-dependent phenotypes are driven not only by alterations in individual cell types but also by the reciprocal interactions between CM and cMSC, which may further impact disease pathogenesis. We utilized a patient-specific, multicellular cardiac system composed of either control or PKP2-mutated CM and cMSC to assess the mutation’s role in fibro-fatty phenotype by immunofluorescence, and contractile behaviour of co-cultures using cell motion detection software. Additionally, we investigated reciprocal interactions both in silico and via multi-targeted proteomics. We demonstrated that ACM CM can promote fibro-adipose differentiation of cMSC. Conversely, ACM cMSC contribute to increasing the rate of abnormal contractile events with likely arrhythmic significance. Furthermore, we showed that an ACM-causative mutation alters the CM-cMSC interaction pattern. We identified the CM-sourced DLK1 as a novel regulator of fibro-adipose remodelling in ACM. Our study challenges the paradigm of exclusive cell-specific mechanisms in ACM. A deeper understanding of the cell-cell influence is crucial for identifying novel therapeutic targets for ACM, and this concept is exploitable for other cardiomyopathies.
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c-MSCs harboring DGVs can promote fibro-adipogenic differentiation through bidirectional paracrine signaling.
“Cardiac mesenchymal stromal cells (c-MSCs) that harbor DGVs can promote fibro-adipogenic differentiation through bidirectional paracrine signaling [100].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [100]
The Introduction (page unavailable) describes c-MSCs affected by desmosomal mutations and reciprocal, partly paracrine interactions with cardiomyocytes. But the Results section on fibro-adipose differentiation says ACM cardiomyocytes promoted that differentiation in c-MSCs; the Discussion (page unavailable) instead links ACM c-MSCs’ influence on cardiomyocytes to dysfunction. The paper does not establish that mutation-bearing c-MSCs promote fibro-adipogenic differentiation through bidirectional paracrine signaling. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe DLK1-NOTCH pathway is critical for this differentiation; DLK1 suppresses adipogenic differentiation in healthy cardiomyocytes, and ACM cardiomyocytes showed reduced DLK1 levels and thus promoted adipogenic differentiation.
“The DLK1-NOTCH pathway is critical for this differentiation, as DLK1 suppresses adipogenic differentiation in healthy cardiomyocytes, and ACM cardiomyocytes showed reduced DLK1 levels and thus promoted adipogenic differentiation [100].”
From A Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease (2026) · cites this paper as [100]
In Results (‘DLK1 modulates fibro-adipose accumulation of ACM stromal cells’), DLK1 expression is higher in healthy than ACM cardiomyocytes, and added DLK1 reduces lipid accumulation in ACM stromal cells. The paper does not show DLK1 suppressing adipogenic differentiation *in healthy cardiomyocytes*: the differentiating cells are stromal cells. It also proposes, rather than establishes, that reduced cardiomyocyte DLK1 causes their increased differentiation. (LLM, conf=0.88)
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Self-citationA Paradigm Shift: Arrhythmogenic Cardiomyopathy Is an Inflammatory Disease
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Lippi, M., Moimas, S., Braga, L., Santin, Y., Galotta, A., Giacca, M., Pompilio, G., & Sommariva, E. (2025) · Biomolecules · doi:10.3390/biom15111565
Self-citationDisease models and AAV therapies of PKP2-induced arrhythmogenic cardiomyopathy
Geerlings, L., Carreras, Y. R., & Vermeer, M. C. S. C. (2026) · Molecular Therapy Advances · doi:10.1016/j.omta.2026.201688
- Authors
- Maione, A. S., Iengo, L., Sala, L., Massaiu, I., Chiesa, M., Lippi, M., Ghilardi, S., Florindi, C., Lodola, F., Zaza, A., Tondo, C., Schiavone, M., Banfi, C., Pompilio, G., Poggio, P., & Sommariva, E.
- Affiliations
- Centro Cardiologico Monzino (IT)
- IRCCS Istituto Auxologico Italiano (IT)
- University of Milano-Bicocca (IT)
- University of Milan (IT)
- University of Rome Tor Vergata (IT)
- Corresponding author
- Maione, Angela Serena
- ORCID
- Venue
- Cell Death Discovery
- Published
- 2024-11-28
- Volume
- 10
- Issue
- 1
- Pages
- 484-484
- ISSN
- 2058-7716 (ISSN-L)
- PMC
- PMC11604953
- OpenAlex
- W4404794536
- Cited by
- 4
- References
- 73
- Citations by year
- 2026: 2 · 2025: 2
- FWCI
- 1.20
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Death Discovery (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- BOA (University of Milano-Bicocca) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Ministero della Salute
- 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, PKP2 mutation, cardiac mesenchymal stromal cells, DLK1, Notch signaling, cardiomyocyte contractility, desmosomal gene mutations, cell-cell interactions
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.
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