Inside AFAR
Inside AFAR

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Dec 8
5:08 pm

Grantee Spotlight Interview: Changhan David Lee View MoreBACK

AFAR’s grant programs in the biology of aging are central to our mission to support and advance healthy aging through biomedical research. At leading institutions nationwide, our grantees hard work, ingenuity, and leadership are advancing cutting-edge research that will help us all live healthier, longer. AFAR grantees are making this the age of aging better.

In this Grantee Spotlight interview, Changhan David Lee, PhD, shares what inspired him to enter the field of aging research and what impact he hopes his research will make thanks to AFAR’s support. 

Changhan David Lee, PhD

Assistant Professor of Gerontology,
USC, Davis

2016 AFAR Research Grant for Junior Faculty



What inspired you to get into aging research?

Physiological deteriorations that occur with time are often collectively referred to as the “aging process”, and aging is the major risk factor for many diseases. As long as I can remember, I liked the comprehensiveness of the field and the sense that aging research may unveil the fundamental processes of life. It was exhilarating that science was finally revealing the secrets of aging, an ancient quest that was only the topic of numerous myths. Understanding the biology of aging seemed, and still seems, to be a paradigm-shifting and a logical approach to improving human health.

How will AFAR’s support further your research at this point in your career?

Advocacy and funding for aging research are somewhat limited compared to those for major diseases. Research funding is highly competitive, especially for newly minted junior faculty. AFAR has been a major advocate and sponsor for aging research and is a pillar of the aging field that nurtured countless discoveries. As one who studies mitochondria, AFAR is my laboratory’s mitochondria that supports the evolution of our research – it powers our laboratory in various ways.

What’s exciting about your research’s potential impact?

Mitochondria have long been thought as the cellular powerhouse that generates the great majority of our energy. But it is now clear that they also coordinate various cellular activities by actively communicating with the rest of the cell, especially the nucleus. Notably, mitochondria possess their own independent genome and genetic system that presumably originated from symbiotic bacteria (i.e. we have two genomes – nuclear and mitochondrial). We, and others, have found that the mitochondrial genome encodes previously unknown small peptides that have significant biological roles. We focus on one such mitochondrial-derived peptide, MOTS-c, whose expression declines with age and, when injected in older mice, can reverse age-dependent insulin resistance. We strive to identify the exact role of MOTS-c in aging and its translational potential to improve aging metabolism. This may be an unprecedented opportunity to mine the other half of our genomes (i.e. mitochondrial genome) for ancient mitochondrial pro-longevity genes, biomarkers of aging, and therapeutic/diagnostic targets to delay the aging process and prevent/treat age-related diseases.

In three sentences, how would you describe your research?

We have two genomes in our body – the mitochondrial and the nuclear genome. All known genes that regulate lifespan and healthspan are encoded in the nuclear genome. We strive to explore the other half of our genomes (i.e. the mitochondrial genome), which has been in our blind spot, for novel genes that may influence how we age.