Vishal Gohil, Ph.D., has been recognized for his work to uncover details of mitochondrial energy production and discover therapeutics for the rare but deadly diseases that can occur because of mitochondrial dysfunctions.
Gohil, a professor and scientist in the Texas A&M College of Agriculture and Life Sciences Department of Biochemistry and Biophysics and Texas A&M AgriLife Research, is one of 11 distinguished Texas A&M University faculty honored as 2024 Fellows of the Chancellor’s Enhancing Development and Generating Excellence in Scholarship, EDGES, Fellowship program.
Started by Chancellor John Sharp, the EDGES Fellowship is designed to acknowledge and retain mid-career faculty who demonstrate outstanding achievements in their respective disciplines and have gained national and international acclaim for their work.
Gohil’s contributions, particularly with his explorations of genetic disorders like Menkes disease and the role of copper in mitochondrial metabolism, have earned him wide recognition and numerous accolades.
“Dr. Gohil’s efforts to understand mitochondrial biology exemplify Texas A&M AgriLife’s commitment to transformative life sciences research,” said Jeffrey W. Savell, Ph.D., vice chancellor and dean for Agriculture and Life Sciences. “His dedication to pursuing fundamental knowledge and transforming it into practical, life-saving applications demonstrates his excellence in scholarship and reinforces our mission to advance research in the pursuit of healthier lives and futures.”
Advancements in mitochondrial medicine
Gohil has been a member of the Department of Biochemistry and Biophysics for over a decade. In that time, his research has focused on mitochondria, the cellular powerhouses that convert food into useable energy.
Mitochondrial dysfunction has been linked to various age-related human diseases, including cancer, diabetes and neurodegenerative disorders. Mitochondria are also implicated in several metabolic disorders that typically manifest in newborns and young children.
One such example is Menkes disease, a fatal genetic disorder caused by defects in acquisition and distribution of copper in the body, resulting in its deficiency in the brain. Because copper is critical for mitochondria’s energy production, the copper deficiency impairs neurological development. Children born with Menkes disease have a life expectancy of no more than three years, and there is currently no approved treatment for this lethal disease.
Vishal Gohil, Ph.D. (left), and postdoctoral researcher Mohammad Zulkifli, Ph.D. Gohil has earned numerous accolades and recognitions for his work on mitochondrial biology. (Michael Miller/Texas A&M AgriLife)
Using biological models like yeast, zebrafish, mice and human cell lines, Gohil’s lab investigates the full spectrum of proteins and lipids required by the mitochondrial respiratory chain, the string of chemical reactions needed to produce useable energy within cells. One significant discovery by his lab was a family of proteins essential for delivering copper to a crucial point along the mitochondrial respiratory chain.
Gohil’s team also discovered that an experimental pharmaceutical compound can transport copper to mitochondria of critical organs, including the brain of a mouse model of Menkes disease. Guided by studies from his lab, the Spanish Agency of Medicines and Health Products recently approved the first use of this copper-transporting drug in a child with Menkes disease, where initial results are promising. Thus, his work has given hope to the families of children with Menkes disease and other copper deficiency disorders.
“This work illustrates how fundamental discoveries in mitochondrial copper biology using simple models like yeast can have a significant potential for clinical translation,” Gohil said.
In January, Gohil’s lab received the Maximizing Investigators’ Research Award, MIRA, from the National Institute for General Medical Sciences, a branch of the National Institutes of Health, NIH, to further support his exploration of mitochondrial copper biology and medicine.
