Mitochondrial dysfunction in ACM pathogenesis.
- Project duration: January 2021 - January 2024
- Project status: Approval by the Scientific Committee
- Funding: Provincial Joint Programme – IT-FWF (Province BZ funding / Project)
Arrhythmogenic cardiomyopathy (ACM) is characterized by arrhythmia and progressive fibro-fatty substitution of the cardiac tissue leading to ventricular dysfunction. Previously published research provided convincing evidence for the involvement of Reactive Oxygen Species (ROS) in tissue degeneration, with our preliminary data also supporting a broader role for mitochondria in ACM development. The present project, built as a collaboration between EURAC (EURAC, Bolzano/Bozen, South-Tyrol, Italy) and the Medical University of Innsbruck (MUI, Innsbruck, Austria) will:
1) Provide a detailed analysis of structural and functional mitochondrial changes in human ACM cell models;
2) Assess the contribution of mitochondrial and non-mitochondrial ROS sources to the ACM pathogenesis;
3) Obtain evidence that targeting mitochondria can reverse ACM-associated alterations (i.e. increased lipid accumulation and higher ROS production).
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