Cheol-Gu Lee
Korea University · 生化学・遺伝学・分子生物学
研究室紹介
Professor Cheol-Gu Lee's research lab focuses on the molecular mechanisms of aging and longevity, with a central emphasis on how dietary restriction and pharmacological interventions such as caloric restriction and rapamycin modulate gene expression, metabolism, and mitochondrial function. The lab employs high-throughput 'omics' technologies—particularly transcriptomics and metabolomics—to dissect age-related changes in model organisms like mice and budding yeast, aiming to identify conserved pathways that promote healthy aging. A key research direction involves understanding the interplay between nutrient sensing pathways (e.g., mTOR), mitochondrial homeostasis, and oxidative stress in aging and age-related diseases. The lab also investigates non-traditional interventions such as electro-acupuncture, exploring their systemic effects on immune function and neuroendocrine regulation.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15The gene expression profile of the aging process was analyzed in skeletal muscle of mice. Use of high-density oligonucleotide arrays representing 6347 genes revealed that aging resulted in a differential gene expression pattern indicative of a marked stress response and lower expression of metabolic and biosynthetic genes. Most alterations were either completely or partially prevented by caloric restriction, the only intervention known to retard aging in mammals. Transcriptional patterns of calo
To provide a global analysis of gene expression in the aging heart, we monitored the expression of 9,977 genes simultaneously in 5- and 30-month-old male B6C3F(1) mice by using high-density oligonucleotide microarrays and several statistical techniques. Aging was associated with transcriptional alterations consistent with a metabolic shift from fatty acid to carbohydrate metabolism, increased expression of extracellular matrix genes, and reduced protein synthesis. Caloric restriction (CR) starte
To investigate the effects of electro-acupuncture (EA) treatment on regions remote from the application, we measured cellular, enzymatic, and transcriptional activities in various internal tissues of healthy rats. The EA was applied to the well-identified acupoint ST36 of the leg. After application, we measured the activity of natural killer cells in the spleen, gene expression in the hypothalamus, and the activities of antioxidative enzymes in the hypothalamus, liver and red blood cells. The EA
Rapamycin (RM), a drug that inhibits the mechanistic target of rapamycin (mTOR) pathway and responds to nutrient availability, seemingly mimics the effects of caloric restriction (CR) on healthy life span. However, the extent of the mechanistic overlap between RM and CR remains incompletely understood. Here, we compared the impact of CR and RM on cellular metabolic status. Both regimens maintained intracellular ATP through the chronological aging process and showed enhanced mitochondrial capacit
To characterize gene expression that is dependent on the strength of calorie restriction (CR), we obtained transcriptome at different levels of glucose, which is a major energy and carbon source for budding yeast. To faithfully mimic mammalian CR in yeast culture, we reconstituted and grew seeding yeast cells in fresh 2% YPD media before inoculating into 2%, 1%, 0.5% and 0.25% YPD media to reflect different CR strengths. We collected and characterized 160 genes that responded to CR strength base
Mitochondria play a crucial role in eukaryotic cells; the mitochondrial electron transport chain (ETC) generates adenosine triphosphate (ATP), which serves as an energy source for numerous critical cellular activities. However, the ETC also generates deleterious reactive oxygen species (ROS) as a natural byproduct of oxidative phosphorylation. ROS are considered the major cause of aging because they damage proteins, lipids, and DNA by oxidation. We analyzed the chronological life span, growth ph
Caloric restriction (CR) has been shown to extend lifespan and prevent cellular senescence in various species ranging from yeast to humans. Many effects of CR may contribute to extend lifespan. Specifically, CR prevents oxidative damage from reactive oxygen species (ROS) by enhancing mitochondrial function. In this study, we characterized 33 single electron transport chain (ETC) gene-deletion strains to identify CR-induced chronological lifespan (CLS) extension mechanisms. Interestingly, defects