Corie Farnsley Jul 14, 2025
Steven C. Beering Award winner Douglas C. Wallace, PhD, MD (h.c.), will present "Mitochondrial Medicine: The New Biomedical Reality," Aug. 25 at IU Indianapolis. | Graphic by Corie Farnsley. Photo courtesy of Douglas Wallace.
Douglas Wallace, PhD, MD (honoris causa), and his colleagues are widely recognized for founding the field of human mitochondrial genetics more than 35 years ago. Since then, his groundbreaking work has been reshaping the way scientists think about aging, disease and even the way our bodies respond to viruses like COVID-19.
On Aug. 25, Wallace will share his work with the Indiana University School of Medicine community.
Wallace, the 2025 Steven C. Beering Award winner, will present the lecture, "Mitochondrial Medicine: The New Biomedical Reality," at noon ET at Walther Hall on the IU Indianapolis campus. His lecture will also be presented virtually for those who cannot attend in person. Registration details are below.
Over the past four decades, Wallace's research has transformed scientific understanding of how mitochondria influence health, disease and even human evolution. His work has earned international acclaim for:
Wallace currently leads the Center for Mitochondrial and Epigenomic Medicine at the Children’s Hospital of Philadelphia, where he also holds the Michael and Charles Barnett endowed chair in pediatric mitochondrial medicine and metabolic diseases. He holds a faculty appointment in the department of pediatrics, division of human genetics at the University of Pennsylvania.
Mitochondria are portions of cells that turn nutrients into usable energy, through a process called oxidative phosphorylation. This generates the energy we need to live, which is why mitochondria are often called the "power plants" of human cells.
More than just energy producers, they also play a role in signaling, immunity and even how our genes are expressed.
Mitochondria also have their own DNA, which Wallace and his colleagues discovered comes exclusively from one's mother. This is different from nuclear DNA, which comes from both parents.
Problems with mitochondria can arise from changes in either one’s nuclear DNA (nDNA) or mtDNA, including:
Some people have a mix of normal and mutated mtDNA — a condition called heteroplasmy. The balance between normal and mutated mtDNA can affect how well mitochondria work and may influence how genes in the rest of our DNA are turned on or off.
To explore how mtDNA affects health, Wallace’s team studied mice that all had the same nuclear DNA but different mitochondrial haplogroups (the ancient variations mentioned earlier). The mice showed differences in:
One group of mice, with a mitochondrial type called mtDNAZB, produced more mitochondrial reactive oxygen species (mROS) than others. mROS are natural byproducts of oxidative phosphorylation, the process cells use to generate energy. These molecules can help with cell signaling, but they can also cause damage if levels get too high.
Wallace's group found that these mice were more resistant to both cancer and transplanted organs, because the extra mROS damaged a type of immune cell called T regulatory cells (Tregs). Tregs normally keep the immune system in check, but with fewer Tregs, the immune system became more aggressive at attacking tumors and foreign tissues, including transplanted organs.
Wallace's team used mice genetically modified to express the human ACE2 receptor (a protein that regulates blood pressure, fluid balance and inflammation), which made them susceptible to COVID-19 when injected with the SARS-CoV2 virus. Mice with the same mtDNAZB mitochondrial type mentioned above were more resistant to severe disease, again due to the loss of Tregs. In this case, though, the aggressive immune response led to dangerous inflammation. To avoid a lethal cytokine storm — in which a hyper-activated immune system floods the body with pro-inflammatory proteins — a phenomenon that has been common in severe COVID-19 cases, Wallace's team used a special antioxidant enzyme called mCAT and an antioxidant drug called EUK8. Both helped reduce inflammation and protect the lungs, showing that tweaking mitochondrial function could be a powerful way to treat disease.
Wallace's work shows that even small differences in mtDNA can have significant impacts on one’s health. These insights are paving the way for advances in personalized medicine, helping scientists understand why some people get sick while others stay healthy — and how tailoring treatments based on a person's mitochondrial make-up could benefit a patient's long-term prognosis.
Take advantage of the opportunity to learn more about the power plant of the cells and how science can power new possibilities when you attend Wallace's lecture Aug. 25.
Parking is available in the Lockefield or University Hospital parking garages. Parking validation will be provided upon request at event check-in.
* Disclosure: This article was written by Corie Farnsley with support from Microsoft Copilot. Copilot was used primarily to put complex scientific information into lay terms.
Corie is communications generalist for Indiana University School of Medicine Faculty Affairs and Professional Development (FAPD). She focuses on telling the story of FAPD by sharing information about the many opportunities the unit provides for individuals’ professional development, the stories behind how these offerings help shape a broad culture of faculty vitality, and ultimately the impact IU School of Medicine faculty have on the future of health. She is a proud IU Bloomington School of Journalism alumna who joined the IU School of Medicine team in 2023 with nearly 25 years of communications and marketing experience.
