Calpain Inhibition in a Transgenic Model of Calpastatin Overexpression Facilitates Reversal of Myocardial Hypertrophy
Our data demonstrate that calpain-mediated cleavage results in nuclear accumulation of a truncated, constitutively active and degradation-resistant calcineurin isoform that sustains a long-term myocardial hypertrophic response to angiotensin-II beyond withdrawal of the stimulus. Cardiomyocyte specific calpain inhibition by transgenic calpastatin overexpression prevented the post-stimulus myocardial hypertrophic response.
Authors
- Philipp Hillmeister (ORCID: https://orcid.org/0000-0003-1749-2315)
- Nikolaos Pagonas
- Peter Nordbeck (ORCID: https://orcid.org/0000-0002-2560-4068)
- G. Sachse (ORCID: https://orcid.org/0000-0001-5096-4922)
- Ivo Buschmann
- Martin Czolbe
- Joachim P. Schmitt (ORCID: https://orcid.org/0000-0001-5742-1680)
- Daniel Patschan (ORCID: https://orcid.org/0000-0002-6914-5254)
- Johanna Tennigkeit (ORCID: https://orcid.org/0000-0002-5730-0624)
- Oliver Ritter (ORCID: https://orcid.org/0000-0003-2069-4364)
Institutions
- University of Würzburg (DE)
- MRB Research Center for Magnetic Resonance Bavaria (DE)
- Universitätsklinikum Würzburg (DE)
- Medizinische Hochschule Brandenburg Theodor Fontane (DE)
- Universitätsklinikum Brandenburg an der Havel (DE)
- Heinrich Heine University Düsseldorf (DE)
- Brandenburg University of Technology Cottbus-Senftenberg (DE)
Publication Details
- Journal
- ESC Heart Failure
- Published
- 2025-03-02
- DOI
- https://doi.org/10.1002/ehf2.15250
- Citations
- 2
- Primary Topic
- Calpain Protease Function and Regulation
- Type
- article
- Field-Weighted Citation Impact
- 2.30
Funders
- Bundesministerium für Bildung und Forschung