Author

Mario Delmar

New York UniversityORCID 0000-0002-2085-5589Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Approach:experimental assay· 3 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Assay:electrophysiology· 1 Research Focus:gene regulatory network inference· 1 Organism:human· 1

Frequent Co-Authors

Eric M. SmalliD· 2 shared Kavya Phadke· 2 shared Adriana HeguyiD· 1 shared Alan C. BrooksiD· 1 shared Alessandro CospitoiD· 1 shared Benjamin Fisler· 1 shared Cameron D. BakeriD· 1 shared Cynthia A. LoomisiD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 30 mutual co-author links

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2 shared papersCell Biology

Eric M. SmallORCID

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Epicardial contributions to fibro-inflammatory signaling in a Pkp2-deficient arrhythmogenic cardiomyopathy model

Daniel D Han, Alan C. Brooks, Cameron D. Baker, Ronald A Dirkx, Deanne M. Mickelsen, Benjamin Fisler, Kavya Phadke, John M. Ashton, Mario Delmar, Eric M. Small

This study shows that Pkp2 deficiency in epicardium-derived cells leads to fibro-inflammatory signaling and contributes to arrhythmogenic cardiomyopathy pathogenesis.

Circulation Heart Failure · Jun 5, 2026Peer-reviewedCell Biology

Cardiomyocyte-specific plakophilin-2 loss is sufficient to induce aging and senescence of nonmyocytes. Relevance to arrhythmogenic cardiomyopathy.

Giorgia Bertoli, Kavya Phadke, Alessandro Cospito, Joanna Abi Rizk, Mingliang Zhang, Eleni Miliotou, Michael Cammer, Yan Deng, Valeria Mezzano, Mark Alu, Gyles Ward, Cynthia A. Loomis, Adriana Heguy, Feng‐Xia Liang, Eric M. Small, , Mario Delmar

This study shows that loss of PKP2 in cardiomyocytes induces pro-inflammatory senescence in non-myocytes and premature cardiac aging, linking desmosomal arrhythmogenic cardiomyopathy to cellular senescence and aging mechanisms.

Journal of the American Heart Association · Apr 28, 2026Peer-reviewedPhysiology

Electrophysiological abnormalities associated with a CACNA1D variant are rescued by AAV6-Cav1.3-C-terminus gene therapy in patient-iPSC-CMs

Jean‐Baptiste Reisqs, Yvonne Sleiman, Ivan Gando, Michael Cupelli, Vamsi Krishna Murthy Ginjupalli, Hélène Delanoë‐Ayari, William A. Coetzee, Yongxia Sarah Qu, Mario Delmar, Frank Cecchin, Reina Bianca Tan, Mohamed Chahine, Mohamed Boutjdir

This study shows that a CACNA1D variant causes electrophysiological abnormalities in hiPSC-CMs, which are reversed by AAV6-Cav1.3-C-terminus gene therapy.

bioRxiv · Dec 17, 2025 · PreprintPhysiology