William “Sealy” Hambright
  • Department: Linda & Mitch Hart Center for Regenerative and Personalized Medicine

William “Sealy” Hambright,


Principal Investigator & Program Director of Healthy Aging & Diagnostics

As part of Dr. Johnny Huard’s team in the Center for Regenerative Sports Medicine (CRSM), Dr. Hambright’s focus is to develop strategies that target fundamental properties of aging including senescent (aged) cell accumulation, telomere erosion, and inflammation to improve ortho-regenerative medicine therapies. He investigates interventions that encompass four primary pillars: exercise, diet, stem cell-based therapies, and anti-aging compounds including senolytic drugs. He coordinates basic science projects in the Steadman Philippon Research Institute (SPRI) and helps design and initiate clinical studies targeting age-related diseases such as osteoarthritis and osteoporosis. For this role, he helps translate aging-related pre-clinical findings to the clinic by negotiating the regulatory and scientific challenges that exist between. His overarching goal is to provide a combinatorial treatment approach targeting these pillars to improve healthy aging and restore active living.

Dr. Hambright received his B.S. in Biology from the University of Texas at Tyler. He then completed his M.S. Thesis in Microbiology at the University of Texas at Arlington titled: “Using Shewanella baltica Ecotypes as a Model for Transcriptional Variation at the Population Level.”

“I appreciated the smaller classrooms and intimate setting at UT Tyler. I was able to interact with my professors more readily which helped foster my interest in science”

Dr. Hambright’s Ph.D. training was in the Biology of Aging Training Program at UTHealth San Antonio at the Barshop Institute for Longevity and Aging Studies. Under Qitao Ran Ph.D., Sealy investigated the redox biology of age associated neurodegenerative diseases, successfully defending his Dissertation: “Neurodegeneration and Cognitive Impairment Through Elevation of Neuronal Lipid Peroxidation.” He and his colleagues were the first to identify ferroptosis as a novel cell-death mechanism responsible for degeneration of neurons primarily afflicted during ALS and Alzheimer’s disease. His work elucidating these mechanisms in different neuronal populations which has garnered over 200 citations from two different manuscripts.

“I chose to study the biology of aging because it is a principal driver of several debilitating degenerative diseases which collectively represent a significant healthcare burden.”
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