MitoNEET: A Potential Target for Kentucky's Most Pressing Health Issues
Grade Level at Time of Presentation
Sophomore
Major
Biology
Institution 25-26
University of Louisville
KY House District #
28
KY Senate District #
37
Faculty Advisor/ Mentor
Michael Menze
Department
Department of Biology
Abstract
Kentucky has the highest rate of new lung cancer diagnoses nationally (84.1 cases per 100,000 individuals) and ranks among the lowest for patient survival at 26%, according to the American Lung Association. Kentucky also faces a substantial burden from metabolic diseases, including diabetes. The state ranks 9th nationally for diabetes-related mortality, with 14% of adults diagnosed. Together, these diseases account for thousands of deaths annually and place a significant strain on Kentucky’s healthcare system. Improving health outcomes requires not only better treatment but also a deeper understanding of the biological processes that drive disease progression. Many chronic diseases, including cancer and diabetes, are strongly linked to mitochondrial dysfunction, the structures responsible for cellular energy production. However, the cellular mechanisms responsible for maintaining healthy mitochondria remain poorly understood. My research focuses on mitoNEET, a protein on the outer surface of mitochondria that is thought to help regulate cellular energy production and stress, contributing to overall cellular health. We previously found that cells lacking mitoNEET consume significantly less oxygen than normal cells. Because oxygen is essential for mitochondrial energy production, this finding suggests that mitoNEET influences a cell’s energy-generating capacity. To gain further insight, we examined cellular properties and mitochondrial health using flow cytometry, a laboratory technique that allows detailed analysis of individual cells. Mitochondrial stress is closely linked to ferroptosis, a form of cell death that has been associated with cancer, metabolic disease, and aging. Our findings indicate that mitoNEET does not significantly affect this process once cells have reached a point of irreversible damage. Rather, mitoNEET may aid in protection earlier, helping limit the buildup of damage, prompting ongoing studies to investigate this role. By understanding how mitoNEET supports cellular health, this work provides foundational insight that may ultimately guide the development of novel therapeutics for diseases disproportionately impacting Kentucky communities.
MitoNEET: A Potential Target for Kentucky's Most Pressing Health Issues
Kentucky has the highest rate of new lung cancer diagnoses nationally (84.1 cases per 100,000 individuals) and ranks among the lowest for patient survival at 26%, according to the American Lung Association. Kentucky also faces a substantial burden from metabolic diseases, including diabetes. The state ranks 9th nationally for diabetes-related mortality, with 14% of adults diagnosed. Together, these diseases account for thousands of deaths annually and place a significant strain on Kentucky’s healthcare system. Improving health outcomes requires not only better treatment but also a deeper understanding of the biological processes that drive disease progression. Many chronic diseases, including cancer and diabetes, are strongly linked to mitochondrial dysfunction, the structures responsible for cellular energy production. However, the cellular mechanisms responsible for maintaining healthy mitochondria remain poorly understood. My research focuses on mitoNEET, a protein on the outer surface of mitochondria that is thought to help regulate cellular energy production and stress, contributing to overall cellular health. We previously found that cells lacking mitoNEET consume significantly less oxygen than normal cells. Because oxygen is essential for mitochondrial energy production, this finding suggests that mitoNEET influences a cell’s energy-generating capacity. To gain further insight, we examined cellular properties and mitochondrial health using flow cytometry, a laboratory technique that allows detailed analysis of individual cells. Mitochondrial stress is closely linked to ferroptosis, a form of cell death that has been associated with cancer, metabolic disease, and aging. Our findings indicate that mitoNEET does not significantly affect this process once cells have reached a point of irreversible damage. Rather, mitoNEET may aid in protection earlier, helping limit the buildup of damage, prompting ongoing studies to investigate this role. By understanding how mitoNEET supports cellular health, this work provides foundational insight that may ultimately guide the development of novel therapeutics for diseases disproportionately impacting Kentucky communities.