About Sung Min Han
Dr. Han completed his B.S. education in Biotechnology in the Republic of South in 2000. He completed three years of military service in the Republic of Korea Air Force. During master’s training from 2001 to 2003 under the mentorship of Dr. Hyeon-Sook Koo at Yonsei University, South Korea, Dr. Han investigated the role of mitochondria in aging using the nematode C. elegans as a genetic and in vivo model animal. He completed his Ph.D. training in 2012 under the mentorship of Dr. Michael Miller at the University of Alabama at Birmingham Medical School. During his Ph.D. training, he continued to use C. elegans to investigate novel signaling mechanisms that link abnormal mitochondrial function to the mechanisms of amyotrophic lateral sclerosis, a neurodegenerative disorder characterized by a progressive loss of motor neurons. After training in a neurodegenerative disorder, Dr. Han became interested in understanding how the nervous system can restore its function after damage. To this end, Dr. Han joined Dr. Marc Hammarlund’s lab at Yale University to investigate the molecular and cellular mechanisms underlying axon regeneration after neuronal injury. Dr. Han joined the University of Florida in 2018 as an Assistant Professor. He is the Course Director of GMS6893 – Clinical and Translational Science Seminar Series, GMS6622 – Mitochondrial Biology in Aging and Disease, and GMS6771 – Clinical Neuroscience of Aging.
My long-term research goal is to understand (i) how the nervous system retains its function and integrity throughout its lifespan and (ii) how it affects organismal aging and health. My current research goals are to investigate:i) how aging neurons regulate mitochondrial dynamics and localization in response to local demand and injury; ii) how mitochondria control nuclear gene expression in two key conditions, including aging and injury; iii) how mitochondria respond to environmental stress and affect organismal aging and health; iv) how mitochondria stress in the nervous system modulate organismal lifespan and healthspan. We utilize the nematode C. elegans as a powerful genetic and in vivo model to answer these questions.