Author

Stefan Peischard

University Hospital MünsterORCID 0000-0002-1571-9646Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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

Frequent Co-Authors

Guiscard SeebohmiD· 2 shared Andrea Ulrike SteinbickeriD· 1 shared Arie O. VerkerkiD· 1 shared Frank RosenbaueriD· 1 shared Frank SchmelteriD· 1 shared Gonzalo BarrientosiD· 1 shared Gunnar GoergesiD· 1 shared Hugo VerdejoiD· 1 shared

Activity by Year

2024-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersCell Biology

Guiscard SeebohmORCID

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2 papers

Recent·Most cited

Altered dynamics of ATP synthase cause functional irregularities in senescent hiPS-cardiomyocytes

Silke Morris, Nico Marx, Gonzalo Barrientos, Isidora Molina-Riquelme, Frank Schmelter, Hugo Verdejo, Stefan Peischard, Guiscard Seebohm, Verónica Eisner, Karin B. Busch

The paper investigates altered ATP synthase dynamics in senescent hiPS-cardiomyocytes, linking structural changes in mitochondria to reduced enzyme activity and impaired cardiac function.

Aging Cell · Jan 28, 2026Peer-reviewedCell Biology

TMPRSS6 cleaves KCNE1 and causes arrhythmias in iron overload disease

Stefan Peischard, Philipp Kastl, Gunnar Goerges, Julian Alexander Schreiber, Arie O. Verkerk, Ronald Wilders, Paul Disse, Isabelle Hornung, Ursula Klingmüller, Andrea Ulrike Steinbicker, Martina Rauner, Maja Vujić Spasić, Frank Rosenbauer, Sven Guenther Meuth, Thomas Budde, , Guiscard Seebohm

This study identifies TMPRSS6 cleavage of KCNE1 as a mechanism causing arrhythmias in iron overload disease using human iPSC-derived cardiomyocytes and computational models.

bioRxiv · Sep 4, 2024 · PreprintPhysiology