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Epigenetic regulation of Aging "Speed" and "Timing"
We investigates the epigenetic mechanisms that determine the speed and timing of aging. We study how inherited genetic predisposition interacts with environmentally induced epigenetic changes driven by factors such as diet, exercise, sleep, light exposure, inflammation, DNA damage, and physical or psychological stress. By integrating genome-wide and single-cell epigenomic analyses, we aim to understand how age-associated changes in cell-type-specific epigenetic identity contribute to functional decline and age-related diseases. Building on these findings, we identify therapeutic targets and develop interventions that restore or preserve epigenetic integrity, with the ultimate goal of establishing novel strategies for healthy aging, prevention of age-related disorders, and the development of epigenetic-based therapeutics.
Development of a Personalized Healthcare AI Model
We have been developing personalized healthcare AI models that objectively assess and predict individual functional health status by integrating age-related gene expression profiles and proteomic data from humans and mice. We analyze data across a wide range of ages and combine molecular information with multidimensional phenotypes, including muscle strength, cognitive function, physical performance, metabolism, inflammation, and medical imaging. Our goal is to visualize both an individual’s current health condition and the future risk of functional decline. We also aim to predict responses to interventions such as diet, exercise, supplements, and pharmaceuticals, enabling the development of personalized strategies for health maintenance and prevention of age-related decline. Through this work, we seek to establish a next-generation healthcare platform that shifts the focus from disease-centered medicine to the preservation of function, prevention, and extension of healthy lifespan.
Understanding Lifespan Regulation Across Diverse Species
We study a wide variety of organisms with distinct lifespans and life-history strategies, including giant isopods, horned lanternfish, Greenland sharks, webfoot octopuses, giant squids, and penguins. Using comparative genomics, transcriptomics, and proteomics, we investigate the molecular mechanisms underlying exceptional longevity, short lifespan, deep-sea adaptation, unusual reproductive strategies, and diverse life cycles. We aim to identify lifespan-regulating genes, species-specific genetic variants, and molecular networks associated with aging and survival. Promising candidate genes and pathways are then introduced into mouse models or cultured cells to evaluate their functional effects on muscle, cognition, metabolism, immunity, tissue aging, and overall health. By combining comparative biology with experimental validation, we seek to uncover conserved mechanisms of lifespan regulation and translate these findings into new approaches for extending human healthspan and developing interventions against aging.
Physical elasticity and Aging
We investigates how the physical properties of cells and tissues, particularly elasticity and mechanical stiffness, regulate aging and tissue function. Aging is accompanied by progressive changes in the mechanical environment of tissues caused by extracellular matrix remodeling, fibrosis, and alterations in cytoskeletal organization. These biomechanical changes are not merely consequences of aging but actively influence surrounding cells through mechanotransduction pathways, thereby regulating stem cell function, tissue regeneration, inflammation, and cellular senescence. By combining biophysical measurements, molecular biology, and animal models, we aim to elucidate how mechanical signals control the rate of aging and age-related functional decline. Furthermore, we seek to identify mechanosensitive signaling pathways and therapeutic targets that preserve tissue elasticity and restore healthy cellular communication, ultimately contributing to novel interventions for healthy aging and age-related diseases.
Non-visual photoreceptor OPN5 regulates Aging
We investigates the role of the evolutionarily conserved non-visual photoreceptor OPN5 in the regulation of aging and tissue homeostasis. Unlike visual photoreceptors that mediate image formation, OPN5 functions as a light-sensitive signaling molecule expressed in multiple tissues, including the brain, skin, and other peripheral organs. We study how violet light–OPN5 signaling influences circadian biology, metabolism, inflammation, cellular stress responses, and tissue regeneration, and how these processes contribute to healthy aging. Using molecular biology, animal models, and human studies, we aim to uncover the signaling networks downstream of OPN5 and determine whether light can be used as a safe, non-invasive intervention to modulate aging. Our long-term goal is to establish light-based therapeutics that promote healthspan and prevent age-related functional decline by harnessing evolutionarily conserved photoreceptor signaling pathways.
Biotechs
One Genomics
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