Matthew Dodson

I am interested in the cellular and molecular mechanisms that regulate the interplay between metabolism, oxidative stress, mitochondrial function, and autophagy during disease pathogenesis. My PhD dissertation focused on the regulation of autophagy in neurons in response to oxidative and metabolic stress. My current work as a post-doctoral researcher focuses on the link between the Nrf2-Keap1 antioxidant defense pathway and the autophagy-lysosomal pathway during the progression of metabolic diseases linked to chronic exposure to the environmental toxicant arsenic, such as cancer and type II diabetes. Recent work in our lab has shown that arsenic inhibits autophagic flux, resulting in the prolonged activation of the Nrf2-Keap1 pathway. Interestingly, we have also shown that arsenic treatment, or the prolonged activation of Nrf2 in Keap1 knockout cells, also results in mitochondrial fragmentation. I plan to continue investigating the link between the Nrf2-Keap1 pathway and autophagy regulation during increased metabolic and oxidative stress, with a specific emphasis on alterations to mitochondrial function, dynamics and removal via mitophagy. The goal of this work will be to gain a better understanding of how the antioxidant response, mitochondrial health and autophagy are linked, particularly in disease models where metabolic and oxidative dysfunction, are prevalent.  My hope is that my experiences and training as a post-doc will broaden my technical skills and scientific background, helping me to continue to develop my critical and independent thinking skills, obtain independent funding, publish high impact manuscripts, and further my progress toward becoming an independent researcher.