P
P Tirilomis
Researcher at University of Göttingen
Publications - 9
Citations - 283
P Tirilomis is an academic researcher from University of Göttingen. The author has contributed to research in topics: Heart failure & Ryanodine receptor. The author has an hindex of 5, co-authored 9 publications receiving 165 citations.
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Journal ArticleDOI
Empagliflozin directly improves diastolic function in human heart failure
Steffen Pabel,Steffen Pabel,Stefan Wagner,Hannah Bollenberg,Philipp Bengel,Árpád Kovács,Christian Schach,P Tirilomis,Julian Mustroph,André Renner,Jan Gummert,Thomas H. Fischer,Sophie Van Linthout,Carsten Tschöpe,Katrin Streckfuss-Bömeke,Gerd Hasenfuss,Lars S. Maier,Nazha Hamdani,Samuel Sossalla,Samuel Sossalla +19 more
TL;DR: This study aims to investigate whether empagliflozin may cause direct pleiotropic effects on the myocardium, and if so, what mechanisms cause these effects and how they are distributed.
Journal ArticleDOI
Differential regulation of sodium channels as a novel proarrhythmic mechanism in the human failing heart.
Nataliya Dybkova,Shakil Ahmad,Shakil Ahmad,Steffen Pabel,Steffen Pabel,P Tirilomis,Nico Hartmann,Thomas H. Fischer,Philipp Bengel,Theodoros Tirilomis,Senka Ljubojevic,André Renner,Jan Gummert,David Ellenberger,Stefan Wagner,Norbert Frey,Lars S. Maier,Katrin Streckfuss-Bömeke,Gerd Hasenfuss,Samuel Sossalla,Samuel Sossalla +20 more
TL;DR: Involving NaV1.8 inhibition with the specific blockers A-803467 and PF-01247324 decreased INaL, abbreviated APD and reduced cellular-spontaneous Ca2+-release and proarrhythmic events in human failing cardiomyocytes constitutes a promising novel approach for selective anti-arrhythmmic therapy in HF.
Journal ArticleDOI
Sarcoplasmic reticulum calcium leak contributes to arrhythmia but not to heart failure progression.
Belal A. Mohamed,Belal A. Mohamed,Nico Hartmann,P Tirilomis,Karolina Sekeres,Karolina Sekeres,Wener Li,Wener Li,Stefan Neef,Claudia Richter,Claudia Richter,Elisabeth M. Zeisberg,Lars Kattner,Michael Didié,Kaomei Guan,Kaomei Guan,Jan D. Schmitto,Stephan E. Lehnart,Stephan E. Lehnart,Stefan Luther,Stefan Luther,Niels Voigt,Tim Seidler,Samuel Sossalla,Samuel Sossalla,Gerd Hasenfuss,Karl Toischer +26 more
TL;DR: It is suggested that SR Ca2+ leak does not primarily influence contractile HF progression, whereas rycal S36 treatment markedly reduces ventricular arrhythmias, thereby improving survival in mice.
Journal ArticleDOI
Inhibition of NaV1.8 prevents atrial arrhythmogenesis in human and mice.
Steffen Pabel,Shakil Ahmad,Shakil Ahmad,P Tirilomis,Thea Stehle,Julian Mustroph,M Knierim,Nataliya Dybkova,Philipp Bengel,Andreas Holzamer,Michael Hilker,Katrin Streckfuss-Bömeke,Gerd Hasenfuss,Lars S. Maier,Samuel Sossalla,Samuel Sossalla +15 more
TL;DR: In vivo experiments in SCN10A−/− mice showed that genetic ablation of NaV1.8 protects against atrial fibrillation induction and reveals a new selective therapeutic target for treating atrial arrhythmias.
Journal ArticleDOI
The functional consequences of sodium channel NaV1.8 in human left ventricular hypertrophy
Shakil Ahmad,Shakil Ahmad,P Tirilomis,Steffen Pabel,Nataliya Dybkova,Nico Hartmann,Cristina E. Molina,Theodoros Tirilomis,Ingo Kutschka,Norbert Frey,Lars S. Maier,Gerd Hasenfuss,Katrin Streckfuss-Bömeke,Samuel Sossalla,Samuel Sossalla +14 more
TL;DR: In hypertrophy and heart failure, the proarrhythmic persistent Na+ current (INaL) is enhanced and the electrophysiological role of neuronal sodium channel NaV1.8 in human hypertrophied myocardium is investigated.