Yun Soo Hong
Yun Soo Hong
Assistant Professor of Epidemiology
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Professional overview
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Yun Soo Hong is an Assistant Professor in the Department of Epidemiology at the NYU School of Global Public Health. Dr. Hong is a physician epidemiologist who received her medical degree in Ewha Womans University (Seoul), completed her internship and residency in Samsung Medical Center (Seoul), and received her MHS and PhD degrees in epidemiology from the Johns Hopkins Bloomberg School of Public Health (Baltimore). In addition, she completed her postdoctoral training at the Johns Hopkins School of Medicine (Baltimore).
Dr. Hong's research focuses on cardiovascular disease epidemiology, integrating genetics, multi-omics, and environmental exposures to identify novel determinants of cardiometabolic health. She leverages large-scale population-based cohort studies, including the UK Biobank, the All of Us Research Program, the Trans-Omics for Precision Medicine (TOPMed), and the Atherosclerosis Risk in Communities (ARIC) Study, to address critical questions in cardiovascular disease epidemiology and prevention. Dr. Hong’s work (80 original articles) has been published in leading journals including Nature Communications, European Respiratory Journal, Heart, and Journal of Allergy and Clinical Immunology.
At the School of Global Public Health, Dr. Hong is teaching epidemiological methods (Epidemiological Methods and Design), covering different study designs and causal inference methods. Dr. Hong is also a methods consultant editor at Annals of Internal Medicine. Through her work, Dr. Hong aims to advance precision medicine and public health approaches that can inform strategies for cardiovascular and chronic disease prevention and treatment. She is also interested in advancing training and academic programs for master’s and PhD students.
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Education
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MHS, Epidemiology, Johns Hopkins Bloomberg School of Public HealthPhD, Epidemiology, Johns Hopkins Bloomberg School of Public HealthMD, Ewha Womans University
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Publications
Publications
Mitochondrial heteroplasmy is a risk factor for the development of chronic lymphocytic leukemia
AbstractPasca, S., Hong, Y. S. S., Shi, W., Puiu, D., Lake, N. J., Lek, M., Guallar, E., Arking, D. E., Gondek, L. P., & Hong, Y. S. (n.d.).Publication year
2026Journal title
Nature communicationsVolume
17Issue
1AbstractChronic lymphocytic leukemia (CLL) can arise from lymphoid clonal hematopoiesis of indeterminate potential (L-CHIP), but many individuals who develop CLL lack detectable L-CHIP prior to diagnosis. To identify additional predictors of CLL risk, we analyze mitochondrial heteroplasmy in 419,154 individuals from the UK Biobank (UKB). Heteroplasmy is associated with a 1.5-fold increased risk of developing CLL, and this risk rises to 4-fold when accounting for deleterious heteroplasmic variants. These findings are confirmed in an independent cohort, the All of Us Research Program (AoU). Notably, the associations remain significant even in the absence of L-CHIP, highlighting heteroplasmy's potential utility as an independent biomarker. Moreover, heteroplasmy is enriched in individuals with high-risk L-CHIP genotypes and large clonal burden, suggesting a potential biological role in malignant transformation. Here, we show that mitochondrial heteroplasmy, especially functionally deleterious variants, identifies individuals at increased risk of CLL who would otherwise go undetected by L-CHIP-based assessments.Hearing changes and trajectories during the menopausal transition and their association with metabolic factors
AbstractJang, Y., Chang, Y., Lee, J., Seo, B., Cho, Y., Kim, M., Park, J. H. H., Kang, J., Kwon, R., Lim, G.-Y. Y., Kim, K.-H. H., Kim, H., Hong, Y. S. S., Park, J., Zhao, D., Cho, J., Guallar, E., Ryu, S., & Hong, Y. S. (n.d.).Publication year
2025Journal title
MaturitasVolume
201Page(s)
108686AbstractHearing loss is an emerging public health concern, with women typically experiencing deterioration during menopause; however, longitudinal studies across this transition are limited. This study examined hearing changes across the menopausal transition in order to identify distinct patterns of hearing decline from 11 years before to 9 years after the final menstrual period, with the goal of informing strategies for early detection and intervention.Longitudinal patterns and group heterogeneity of depressive symptoms during menopausal transition in middle-aged Korean women
AbstractJang, Y., Chang, Y., Park, J., Jeon, S. W. W., Seo, B., Park, J. H. H., Kang, J., Kwon, R., Lim, G.-Y. Y., Kim, K.-H. H., Kim, H., Hong, Y. S. S., Park, J., Zhao, D., Cho, J., Guallar, E., Ryu, S., & Hong, Y. S. (n.d.).Publication year
2025Journal title
Epidemiology and psychiatric sciencesVolume
34Page(s)
e57AbstractWhile depressive symptoms are common during menopausal transition, the relationship between the two remains unclear. Therefore, this study aimed to examine the longitudinal changes in depressive symptoms among middle-aged Korean women and identify those with elevated and worsening symptoms during this period.Menopausal stage transitions and associations with overall and domain-specific perceived stress in middle-aged Korean women
AbstractJang, Y., Chang, Y., Jeon, S. W. W., Park, J., Seo, B., Kang, J., Kwon, R., Lim, G.-Y. Y., Kim, K.-H. H., Kim, H., Hong, Y. S. S., Park, J., Zhao, D., Cho, J., Guallar, E., Ryu, S., & Hong, Y. S. (n.d.).Publication year
2025Journal title
MaturitasVolume
200Page(s)
108660AbstractThe menopausal transition, closely linked to later-life health, involves substantial physiological and psychological changes, potentially increasing perceived stress. However, longitudinal studies have reported inconsistent results, with limited data for Asian women, despite the potential for perceived stress to vary with both race and socioeconomic status. Therefore, this study investigated the longitudinal association between menopausal transition and perceived stress among middle-aged Korean women.Reversible compromise of physiological resilience by accumulation of heteroplasmic mtDNA mutations
AbstractHuang, H., Wang, Y., Zsengeller, Z. K., Gorham, J. M., Vemireddy, V., Clark, A. J., Pan, H., Dreyfuss, J. M., Jotwani, V., Shlipak, M. G., Sarnak, M. J., Parikh, C. R., Thiessen-Philbrook, H., Katz, R., Waikar, S. S., Lake, N. J., Lek, M., Shi, W., Puiu, D., … Hong, Y. S. (n.d.).Publication year
2025Journal title
Science (New York, N.Y.)Volume
390Issue
6769Page(s)
164-172AbstractSomatically acquired mitochondrial DNA (mtDNA) mutations accumulate with age, but the mechanisms and consequences of this accumulation are poorly understood. Here we show that transient injuries induce a burst of persistent mtDNA mutations that impair resilience to future injuries. mtDNA mutations suppressed energy-intensive nucleotide metabolism. Repletion of adenosine, but not other nucleotides, restored adenosine triphosphate generation, which required a nuclear-encoded purine biosynthetic enzyme, adenylate kinase 4 (AK4). Analysis of 369,912 UK Biobank participants revealed a graded association between mutation burden and chronic kidney disease severity as well as an independent increase in the risk of future acute kidney injury events ( < 10). Heteroplasmic mtDNA mutations may therefore reflect the cumulative effect of acute injuries to metabolically active cells, impairing major functions in a fashion amenable to nuclear-controlled purine biosynthesis.