Elevated levels of Letm1 drives mitochondrial dysfunction and cardiomyocyte stress-mediated apoptosis in cultured cardiomyocytes
Cardiac ischemia, a predominant cause of heart failure, is marked by profound mitochondrial dysfunction, dysregulated ion homeostasis, and maladaptive cellular remodeling, all of which compromise cardiac performance. The mitochondrial inner membrane protein Leucine zipper-EF-hand containing Transmem...
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| Main Authors: | , , , , , , , , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
2025
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| In: |
Cell communication and signaling
Year: 2025, Volume: 23, Pages: 1-24 |
| ISSN: | 1478-811X |
| DOI: | 10.1186/s12964-025-02378-7 |
| Online Access: | Verlag, kostenfrei, Volltext: https://doi.org/10.1186/s12964-025-02378-7
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| Author Notes: | Anushka Deshpande, Leo Weirauch, Tapan Kumar Baral, Marco Steier, Ankush Borlepawar, Manju Kumari, Lucia S. Kilian, Karsten Richter, Elke Hammer, Derk Frank, Constanze Schmidt, Norbert Frey and Ashraf Y. Rangrez |
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| 245 | 1 | 0 | |a Elevated levels of Letm1 drives mitochondrial dysfunction and cardiomyocyte stress-mediated apoptosis in cultured cardiomyocytes |c Anushka Deshpande, Leo Weirauch, Tapan Kumar Baral, Marco Steier, Ankush Borlepawar, Manju Kumari, Lucia S. Kilian, Karsten Richter, Elke Hammer, Derk Frank, Constanze Schmidt, Norbert Frey and Ashraf Y. Rangrez |
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| 520 | |a Cardiac ischemia, a predominant cause of heart failure, is marked by profound mitochondrial dysfunction, dysregulated ion homeostasis, and maladaptive cellular remodeling, all of which compromise cardiac performance. The mitochondrial inner membrane protein Leucine zipper-EF-hand containing Transmembrane Protein 1 (Letm1), implicated in Wolf-Hirschhorn Syndrome, is essential for mitochondrial function. Although genetic alterations in Letm1 are linked to cardiomyopathies, its specific contributions to cardiac pathophysiology, particularly in the context of ischemic heart disease, remain poorly defined. This study aims to elucidate the role of Letm1 in ischemic cardiac pathology and its mechanistic impact on cardiomyocyte function. | ||
| 650 | 4 | |a Arrhythmias | |
| 650 | 4 | |a Cardiomyocytes | |
| 650 | 4 | |a Hypertrophy | |
| 650 | 4 | |a Letm1 | |
| 650 | 4 | |a Mitochondrial metabolism | |
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