Postdoctoral Scholar, University of California San Francisco
Glenn Foundation for Medical Research Postdoctoral Fellowships in Aging Research - 2022
What inspired you to pursue aging research?
As a zygote develops and grows into a large animal, its pool of mitochondrial genomes expands to a mind-blowing number that vastly exceeds the number of individual organisms making up most species. Additionally, in a fully-grown organism this huge population of mitochondrial genomes constantly turns over going through thousands of generations. During these processes mitochondrial genomes compete with each other for replication and transmission. Given the number of replication rounds and high mutational frequency, all possible mutations in mitochondrial genomes will occur billions of times. Each variant genome will have an opportunity to flourish or fail in an intra-organismal evolutionary contest. This staggering perspective inspired me to study evolutionary processes leading to age-dependent erosion of mitochondrial genome and explore how this erosion contributes to aging.
In your view, what does AFAR mean to the field, and what does it mean for you to receive an AFAR grant now?
AFAR promotes innovative research in the aging field. I think it is particularly valuable that AFAR supports young talents that grow to become leaders in the aging field. Their ground-breaking research has a far-reaching impact on human health, getting us closer to a longer healthier life. I am honored that AFAR chose to support my work. This support will help me to pursue my research goals and become an independent investigator.
What is exciting about your research’s potential impact?
Accumulation of mitochondrial genome mutations in somatic tissues was implicated in age-related diseases several decades ago. Yet, to date, it remains elusive how this accumulation causes aging symptoms. Recent advances suggest that mitochondrial genome mutations might cause aging via stress signaling from compromised mitochondria that reverberates to the whole organism. My work will test this idea and identify the stress pathways activated in cells with high levels of mutant mitochondrial genomes. Pharmacological modulation of these pathways might potentially delay age-related degeneration.
How would you describe your research to a non-scientist?
Mitochondria, tiny but mighty “power houses” in our cells, have their own genome that is essential for energy production. With age mitochondrial genome erodes due to progressive accumulation of mutations. This accumulation is thought to cause many age-related diseases including muscle atrophy and Parkinson’s disease. In my work, I am trying to understand how mitochondrial genome mutations contribute to aging.
