Author

A. G. Edwards

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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Physiology· 3 Biophysics· 2 Pharmacology & Toxicology· 2

Signature Assays, Organisms & Methods

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Organism:human· 6 Assay:electrophysiology· 4 Research Focus:cell type annotation· 3 Approach:deep learning· 3 Approach:experimental assay· 3 Approach:statistical model· 3 Research Focus:differential expression· 2 Research Focus:drug response / drug discovery· 2

Frequent Co-Authors

E. Grandi· 3 shared H. Ni· 3 shared S. Morotti· 3 shared A. Tveito· 2 shared C. Smith· 2 shared D. Sato· 2 shared K. H. Jaeger· 2 shared W. E. Louch· 2 shared

Activity by Year

2018-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 22 mutual co-author links

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3 shared papersPhysiology

E. Grandi

Mutual co-authors in cluster

Author profile →

7 papers

Recent·Most cited

The Sodium/Glucose Cotransporter 2 Inhibitor Empagliflozin Inhibits Long QT 3 Late Sodium Currents in a Mutation Specific Manner

L. Lunsonga, M. Fatehi, W. Long, A. Barr, B. E. Gruber, A. Chattopadhyay, K. Barakat, A. G. Edwards, P. E. Light

This paper investigates how empagliflozin affects late sodium currents in specific LQT3 mutations, finding it selectively inhibits these currents in some mutations but not others.

bioRxiv · Apr 15, 2024Pharmacology & Toxicology

Pharmacological or genetic inhibition of Scn9a protects human and mouse beta cells while dampening insulin secretion in type 1 diabetes

P. Overby, A. G. Gordon, X.-Q. Dai, N. S. Nahirney, S. Provenzano, W. G. Sun, Y. Xia, J. A. Zhang, E. Panzhinskiy, C. M. J. Chu, H. H. Cen, S. Skovso, J. Kolic, A. G. Edwards, P. E. Macdonald, J. D. Johnson

This study shows that inhibiting Scn9a protects beta cells in type 1 diabetes by reducing excitability and improving survival, while also dampening insulin secretion.

bioRxiv · Jun 11, 2023 · PreprintPhysiology

Mechanisms of spontaneous Ca2+ release-mediated arrhythmia in a novel 3D human atrial myocyte model: II. Ca2+-handling protein variation

X. Zhang, C. Smith, S. Morotti, A. G. Edwards, D. Sato, W. E. Louch, H. Ni, E. Grandi

This paper uses a 3D human atrial myocyte model to study how changes in Ca2+-handling proteins and TATS density affect arrhythmia mechanisms in disease.

bioRxiv · Jul 15, 2022Physiology

Mechanisms of spontaneous Ca2+ release-mediated arrhythmia in a novel 3D human atrial myocyte model: I. Transverse-axial tubule variation

X. Zhang, H. Ni, S. Morotti, C. Smith, D. Sato, W. E. Louch, A. G. Edwards, E. Grandi

This study develops a 3D human atrial myocyte model to investigate how variations in transverse-axial tubule systems (TATS) affect Ca2+ handling and promote arrhythmia through spontaneous Ca2+ release.

bioRxiv · Jul 15, 2022Physiology

Mutations change excitability and the probability of re-entry in a computational model of cardiac myocytes in the sleeve of the pulmonary vein

K. H. Jaeger, A. Tveito, W. Giles, A. G. Edwards

The paper uses a computational model to study how AF-associated mutations affect ectopic beats and re-entry in the pulmonary vein-left atrium transition region.

bioRxiv · Sep 24, 2021 · PreprintBiophysics

Sex-specific classification of drug-induced Torsade de Pointes susceptibility using cardiac simulations and machine learning

A. Fogli Iseppe, H. Ni, S. Zhu, X. Zhang, R. Coppini, P.-C. Yang, U. Srivatsa, C. E. Clancy, A. G. Edwards, S. Morotti, E. Grandi

This paper develops sex-specific TdP risk classifiers using cardiac simulations and machine learning, finding that male-based models underestimate female TdP risk.

Clinical Pharmacology & Therapeutics · Apr 19, 2021Peer-reviewedPharmacology & Toxicology

Inversion and computational maturation of drug response using human stem cell derived cardiomyocytes in microphysiological systems

A. Tveito, K. H. Jaeger, N. Huebsch, B. Charrez, A. G. Edwards, S. Wall, K. E. Healy

This paper develops a computational framework to predict drug effects in mature cardiomyocytes using data from immature human stem cell-derived cardiomyocytes in microphysiological systems.

bioRxiv · Jul 10, 2018Biophysics