Florian J. G. Waleczek
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Florian J. G. Waleczek has a total of 23 co-authors. Here are the top co-authors by number of shared publications:
- Natalie Weber
Institute of Molecular and Translational Therapeutic Strategies (IMTTS) Hannover Medical School Hannover Germany
2 shared publications - Thomas Thum
Institute of Molecular and Translational Therapeutic Strategies, Hannover Medical School, Hannover, Germany
2 shared publications - Alfredo Jesús López-Dávila
Institute of Molecular and Cell Physiology, Hannover Medical School, Hannover 30625, Germany
1 shared publication - Andreas Pich
Institute of Toxicology and Core Facility Proteomics, Hannover Medical School, Hannover, Germany
1 shared publication - Angelika Pfanne
Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, 30625 Hannover, Germany
1 shared publication - Ankita Garg
Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, 30625 Hannover, Germany
1 shared publication
Latest Publications
- Open Access
- 20 January 2026
- Published by Elsevier in Biomedicine & Pharmacotherapy
- Vol. 195, 119017
Pharmacological inhibition of myosin reduces the cytotoxic effect of a Lys49 PLA2-like myotoxin on human and rat cardiac muscle
- 20 January 2026
- Published by Elsevier in Biomedicine & Pharmacotherapy
- Vol. 195, 119017
Open AccessPharmacological inhibition of myosin reduces the cytotoxic effect of a Lys49 PLA2-like myotoxin on human and rat cardiac muscle
- Open Access
- 30 December 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 26 (1) , 218
Prolonged Hypoxia in Rat Living Myocardial Slices Affects Function, Expression, and Structure
Ischemic heart disease is the leading cause of death worldwide. Reduced oxygen supply and myocardial hypoxia lead to tissue damage and impairment of the heart function. To the best of our knowledge, the primary functional effects of hypoxia in the multicellular model of living myocardial slices (LMSs) have not been investigated so far. In this study, we analyzed force generation, ultrastructure, gene expression, and proteome changes in rat LMS after 24 h of ex vivo culture in normal and reduced levels of oxygen (O2). We observed a significant reduction in absolute force and a slowdown of force kinetics as well as an increase in cardiomyocyte apoptosis and myofibrillar and mitochondrial damage, as well as transcriptomic changes. Proteome analysis revealed the deregulation of proteins involved in metabolic processes, hypoxic response, and neutralizing of reactive oxygen species. Our results indicate that hypoxia induces substantial primary changes in heart tissue, which are independent of perfusion and immune responses. Our new LMS model could serve as a screening system for drug development and new mechanistic insights.
- 30 December 2024
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 26 (1) , 218
Open AccessProlonged Hypoxia in Rat Living Myocardial Slices Affects Function, Expression, and Structure
Ischemic heart disease is the leading cause of death worldwide. Reduced oxygen supply and myocardial hypoxia lead to tissue damage and impairment of the heart function. To the best of our knowledge, the primary functional effects of hypoxia in the multicellular model of living myocardial slices (LMSs) have not been investigated so far. In this study, we analyzed force generation, ultrastructure, gene expression, and proteome changes in rat LMS after 24 h of ex vivo culture in normal and reduced levels of oxygen (O2). We observed a significant reduction in absolute force and a slowdown of force kinetics as well as an increase in cardiomyocyte apoptosis and myofibrillar and mitochondrial damage, as well as transcriptomic changes. Proteome analysis revealed the deregulation of proteins involved in metabolic processes, hypoxic response, and neutralizing of reactive oxygen species. Our results indicate that hypoxia induces substantial primary changes in heart tissue, which are independent of perfusion and immune responses. Our new LMS model could serve as a screening system for drug development and new mechanistic insights.