Author

R. Doste

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Bioengineering· 2 Physiology· 1

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 3 Approach:experimental assay· 3 Organism:human· 3 Research Focus:cell type annotation· 2 Assay:electrophysiology· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell-cell communication· 1 Approach:deep learning· 1

Frequent Co-Authors

A. Bueno-Orovio· 2 shared B. Rodriguez· 2 shared Z. J. Wang· 2 shared A. Garfinkel· 1 shared C. N. Toepfer· 1 shared C. Seidman· 1 shared C. Trovato· 1 shared F. Margara· 1 shared

Activity by Year

2022-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 33 mutual co-author links

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2 shared papersBioengineering

A. Bueno-Orovio

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

In Silico Evaluation of Cell Therapy in Acute versus Chronic Infarction: Role of Automaticity, Heterogeneity and Purkinje in Human

L. L. Riebel, Z. J. Wang, H. Martinez-Navarro, C. Trovato, J. Camps, L. A. Berg, X. Zhou, R. Doste, R. Sachetto Oliveria, R. Weber dos Santos, J. Biasetti, B. Rodriguez

The paper uses human-based modeling to evaluate cell therapy in acute and chronic myocardial infarction, finding that cell heterogeneity and Purkinje system function influence arrhythmia risk.

bioRxiv · Dec 11, 2023Bioengineering

Human iPSC-CMs and in-silico technologies define mechanisms and accelerate targeted pharmacogenetics in hypertrophic cardiomyopathy

F. Margara, Y. Psaras, Z. J. Wang, M. Schmid, R. Doste, A. Garfinkel, G. G. Repetti, J. Seidman, C. Seidman, B. Rodriguez, C. N. Toepfer, A. Bueno-Orovio

The paper combines human iPSC-CMs and in-silico models to identify genotype-specific pathomechanisms and therapeutic targets in hypertrophic cardiomyopathy.

bioRxiv · Jun 8, 2022 · PreprintBioengineering

Remodelling of potassium currents underlies arrhythmic action potential prolongation under beta-adrenergic stimulation in hypertrophic cardiomyopathy

R. Doste, R. Coppini, A. Bueno-Orovio

This study identifies reduced potassium currents as the main mechanism of action potential prolongation in HCM under beta-adrenergic stimulation, leading to arrhythmogenic risks.

bioRxiv · Mar 1, 2022Physiology