Hyon‐Seung Yi

ORCID: 0000-0002-3767-1954
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About
Contact & Profiles
Research Areas
  • Nutrition and Health in Aging
  • Liver Disease Diagnosis and Treatment
  • GDF15 and Related Biomarkers
  • Thyroid Cancer Diagnosis and Treatment
  • Thyroid and Parathyroid Surgery
  • Adipokines, Inflammation, and Metabolic Diseases
  • Adipose Tissue and Metabolism
  • Cancer, Hypoxia, and Metabolism
  • Liver physiology and pathology
  • Endoplasmic Reticulum Stress and Disease
  • Liver Diseases and Immunity
  • Mitochondrial Function and Pathology
  • Thyroid Disorders and Treatments
  • Fibroblast Growth Factor Research
  • Diet, Metabolism, and Disease
  • Diabetes and associated disorders
  • Parathyroid Disorders and Treatments
  • Macrophage Migration Inhibitory Factor
  • Nuclear Receptors and Signaling
  • Immune Cell Function and Interaction
  • Diet and metabolism studies
  • Immune cells in cancer
  • Atherosclerosis and Cardiovascular Diseases
  • BRCA gene mutations in cancer
  • Extracellular vesicles in disease

Chungnam National University
2016-2025

Wonkwang University
2025

Winthrop-University Hospital
2025

National University College
2020-2024

New Generation University College
2020-2024

Chungnam National University Hospital
2016-2024

Korea Advanced Institute of Science and Technology
2012-2024

Kyushu University Hospital
2024

Research Institute for Endocrine Sciences
2024

Gachon University
2009-2015

Reduced mitochondrial electron transport chain activity promotes longevity and improves energy homeostasis via cell-autonomous –non-autonomous factors in multiple model systems. This mitohormetic effect is thought to involve the unfolded protein response (UPRmt), an adaptive stress-response pathway activated by proteotoxic stress. Using mice with skeletal muscle–specific deficiency of Crif1 (muscle-specific knockout [MKO]), integral large mitoribosomal subunit (39S), we identified growth...

10.1083/jcb.201607110 article EN cc-by-nc-sa The Journal of Cell Biology 2016-12-16

Abstract Reactive oxygen species (ROS) contribute to the development of non-alcoholic fatty liver disease. ROS generation by infiltrating macrophages involves multiple mechanisms, including Toll-like receptor 4 (TLR4)-mediated NADPH oxidase (NOX) activation. Here, we show that palmitate-stimulated CD11b + F4/80 low hepatic macrophages, but not high Kupffer cells, generate via dynamin-mediated endocytosis TLR4 and NOX2, independently from MyD88 TRIF. We demonstrate differently LPS-mediated...

10.1038/s41467-017-02325-2 article EN cc-by Nature Communications 2017-12-15

Non-alcoholic fatty liver disease (NAFLD) is a dominant cause of chronic disease, but the exact mechanism progression from simple steatosis to nonalcoholic steatohepatitis (NASH) remains unknown. Here, we investigated role exosomes in NAFLD progression. Exosomes were isolated human hepatoma cell line treated with palmitic acid (PA) and their miRNA profiles examined by microarray. The hepatic stellate (HSC) (LX-2) was then exosome hepatocytes. Compared controls, PA-treated hepatocytes...

10.1038/s41598-017-03389-2 article EN cc-by Scientific Reports 2017-06-12

During liver injury, hepatocytes secrete exosomes that include diverse types of self‐RNAs. Recently, self‐noncoding RNA has been recognized as an activator Toll‐like receptor 3 (TLR3). However, the roles hepatic and TLR3 in fibrosis are not yet fully understood. Following acute injury early‐stage induced by a single or 2‐week injection carbon tetrachloride (CCl 4 ), increased interleukin (IL)‐17A production was detected primarily γδ T cells wild‐type (WT) mice. IL‐17A were both significantly...

10.1002/hep.28644 article EN Hepatology 2016-05-14

Oxidative functions of adipose tissue macrophages control the polarization M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with mitochondrial phosphorylation (OxPhos) due to myeloid-specific deletion CR6-interacting factor 1 (Crif1), an essential mitoribosomal involved biogenesis OxPhos subunits, have inflammation. Macrophage GDF15 expression impaired function, induced upon...

10.1038/s41467-018-03998-z article EN cc-by Nature Communications 2018-04-13

To date, no pharmacological therapy has been approved for non-alcoholic fatty liver disease (NAFLD). The aim of the present study was to evaluate therapeutic potential poly ADP-ribose polymerase (PARP) inhibitors in mouse models NAFLD.As ADP-ribosylation (PARylation) proteins by PARPs consumes nicotinamide adenine dinucleotide (NAD+), we hypothesized that overactivation drives NAD+ depletion NAFLD. Therefore, assessed effectiveness PARP inhibition replenish and activate NAD+-dependent...

10.1016/j.jhep.2016.08.024 article EN cc-by-nc-nd Journal of Hepatology 2016-09-21

Abstract Mitochondrial dysfunction is associated with aging‐mediated inflammatory responses, leading to metabolic deterioration, development of insulin resistance, and type 2 diabetes. Growth differentiation factor 15 (GDF15) an important mitokine generated in response mitochondrial stress dysfunction; however, the implications GDF15 aging process are poorly understood mammals. In this study, we identified a link between stress‐induced production protection from tissue inflammation on humans...

10.1111/acel.13195 article EN cc-by Aging Cell 2020-07-21

Abstract Growth differentiation factor 15 (GDF15) has recently been shown to have an important role in the regulation of mitochondrial function and pathogenesis complex human diseases. Nevertheless, GDF15 alcohol-induced or fibrotic liver diseases yet be determined. In this study, we demonstrate that alcohol- carbon tetrachloride (CCl 4 )-mediated hepatic production ameliorates inflammation fibrosis. Alcohol directly enhanced expression primary hepatocytes, which led increased oxygen...

10.1038/s41598-017-17574-w article EN cc-by Scientific Reports 2017-12-04

Abstract Chronic inflammation is a driving force for the development of metabolic disease including diabetes and obesity. However, functional characteristics T-cell senescence in abnormal glucose homeostasis are not fully understood. We studied patients visiting hospital routine health check-ups, who were divided into two groups: normal controls people with prediabetes. Gene expression profiling peripheral blood mononuclear cells from type 2 was undertaken using microarray analysis. also...

10.1038/s41419-019-1494-4 article EN cc-by Cell Death and Disease 2019-03-13

Perturbation of mitochondrial proteostasis provokes cell autonomous and non-autonomous responses that contribute to homeostatic adaptation. Here, we demonstrate distinct metabolic effects hepatic metabokines as factors in mice with OxPhos dysfunction. Liver-specific stress induced by a loss-of-function mutation Crif1 (LKO) leads aberrant oxidative phosphorylation promotes the unfolded protein response. LKO are highly insulin sensitive resistant diet-induced obesity. The hepatocytes secrete...

10.1016/j.isci.2021.102181 article EN cc-by iScience 2021-02-16

Sirtuin 7 (SIRT7) plays an important role in tumor development, and has been characterized as a potent regulator of cellular stress. However, the effect SIRT7 on sorafenib acquired resistance remains unclear possible anti-tumor mechanism beyond this process HCC not clarified. We examined therapeutic potential determined whether it functions synergistically with to overcome chemoresistance.

10.1016/j.drup.2024.101054 article EN cc-by-nc-nd Drug Resistance Updates 2024-01-17

Actin antagonists have previously been shown to alter responses of Commelina communis stomata physiological stimuli, implicating actin filaments in the control guard cell volume changes (M. Kim, P.K. Hepler, S.-O. Eun, K.S. Ha, Y. Lee [1995] Plant Physiol 109: 1077-1084). Since K+ channels play an important role stomatal movements, we examined possible regulation K+-channel activities by state polymerization. Agents affecting polymerization altered light-induced opening and inward measured...

10.1104/pp.115.2.335 article EN PLANT PHYSIOLOGY 1997-10-01

Hypocalcemia and hyperphosphatemia are encountered in idiopathic hypoparathyroidism (IHP) pseudohypoparathyroidism type Ib (PHP1B). In contrast to PHP1B, which is caused by resistance toward parathyroid hormone (PTH), the genetic defects leading IHP impair production of this important regulator mineral ion homeostasis. So far, only five PTH mutations were shown cause IHP, each located hormone's pre-pro leader segment thus secretion. three siblings affected we now identified a homozygous...

10.1002/jbmr.2532 article EN Journal of Bone and Mineral Research 2015-04-18

T-helper type 2 (Th2) cytokines, including interleukin (IL)-13 and IL-4, produced in adipose tissue, are critical regulators of intra-adipose systemic lipid glucose metabolism. Furthermore, IL-13 is a potential therapy for insulin resistance obese mouse models. Here, we examined mediators by adipocytes that responsible regulating homeostasis response to Th2 cytokines. We used RNA sequencing data analysis cultured screen factors secreted recombinant IL-13. Recombinant induced expression...

10.2337/db17-0333 article EN Diabetes 2017-09-05

Several classes of antibiotics have long been known to beneficial effects that cannot be explained strictly on the basis their capacity control infectious agent. Here, we report tetracycline antibiotics, which target mitoribosome, protected against sepsis without affecting pathogen load. Mechanistically, found mitochondrial inhibition protein synthesis perturbed electron transport chain (ETC) decreasing tissue damage in lung and increasing fatty acid oxidation glucocorticoid sensitivity...

10.1016/j.immuni.2020.09.011 article EN cc-by-nc-nd Immunity 2020-10-14

Significance Sepsis remains a leading cause of death. New insights into its pathophysiology are likely to be key the development effective therapeutic strategies against sepsis. Given role GDF15 in metabolism regulation and cachexia during late stages cancer, features that also occur sepsis, elucidation possible mechanistic sepsis is great importance. We find septic patients have very high levels peripheral blood, which correlate with clinical outcomes. Using Gdf15 -deficient mice, we show...

10.1073/pnas.1918508117 article EN cc-by Proceedings of the National Academy of Sciences 2020-05-18

Mitochondrial stress and the dysregulated mitochondrial unfolded protein response (UPR<sup>mt</sup>) are linked to various diseases, including metabolic disorders, neurodegenerative cancer. Mitokines, signaling molecules released by UPR<sup>mt</sup>, crucial mediators of inter-organ communication influence systemic physiological processes. In this review, we provide a comprehensive overview mitokines, their regulation exercise lifestyle interventions implications for...

10.4093/dmj.2023.0115 article EN cc-by-nc Diabetes & Metabolism Journal 2024-01-04
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