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As a member of a multidisciplinary team, Heidi McBride contributes her expertise in cell biology and mitochondrial dysfunction, focusing on the complex pathogenesis of motor neuron degenerative diseases. Her laboratory employs complementary approaches to understand how hundreds of mitochondria within a cell behave as an interconnected group and how their interaction affects cellular function and tissue health. Mitochondria, once thought to solely disturb cellular homeostasis, are now recognized as dynamic structures that can fuse, branch, and split apart. Mutations in mitochondrial proteins can lead to serious degenerative diseases, with implications for the plasticity of these organelles linked to the removal of damaged sections of proteins and lipids. Mitochondrial dysfunction has been associated with diseases such as Amyotrophic Lateral Sclerosis and Parkinson's disease. By characterizing mitochondrial behavior, McBride aims to identify new therapeutic strategies for treating these degenerative conditions. Her research also investigates the mechanisms of mitochondrial fusion, the role of SUMOylation in mitochondrial fission, and the characterization of mitochondrial-derived vesicles, which carry specific protein and lipid cargo to distinct intracellular destinations, thereby opening new avenues for understanding their transport mechanisms and the consequences of pathway failures.
Department: Department of Medicine. Program: Experimental Medicine.