c-Src Is Responsible for Mitochondria-Mediated Arrhythmic Risk in Ischemic Cardiomyopathy
MI leads to increased c-Src active form that results in MCU tyrosine phosphorylation, increased mitochondrial Ca<sup>2+</sup> uptake, QT prolongation, and arrhythmia, suggesting c-Src or MCU may represent novel antiarrhythmic targets.
Authors
- Samuel C. Dudley (ORCID: https://orcid.org/0000-0001-5843-5961)
- Hong Liu (ORCID: https://orcid.org/0000-0002-4079-6985)
- Gyeoung-Jin Kang (ORCID: https://orcid.org/0000-0003-0646-9187)
- Feng Feng (ORCID: https://orcid.org/0000-0001-9912-4318)
- An Xie
- Eun Ji Kim (ORCID: https://orcid.org/0000-0002-3271-1419)
Institutions
- University of Minnesota (US)
- Minneapolis Heart Institute Foundation (US)
Publication Details
- Journal
- Circulation Arrhythmia and Electrophysiology
- Published
- 2024-08-30
- DOI
- https://doi.org/10.1161/circep.124.013054
- Citations
- 5
- Primary Topic
- Mitochondrial Function and Pathology
- Type
- article
- Field-Weighted Citation Impact
- 1.17
Funders
- National Institutes of Health