Sungkyunkwan University · 医学
Professor Byung Jin Kim's research lab focuses on the pathophysiology of metabolic and ocular diseases, with a primary emphasis on the role of zinc signaling in pancreatic beta-cell death and retinal ischemia/reperfusion injury. The lab investigates cellular stress pathways, particularly the JNK signaling cascade, in neurodegenerative conditions such as retinal ganglion cell degeneration. Additionally, the lab explores the metabolic consequences of lifestyle factors, including smoking cessation and alcohol consumption, in relation to metabolic syndrome and non-alcoholic fatty liver disease (NAFLD). These studies integrate molecular biology, in vivo models, and clinical epidemiology to identify novel therapeutic targets.
Figures are computed from collected data and may differ slightly.
Retinal ischemia/reperfusion (I/R) injury is an important cause of visual impairment. However, questions remain on the overall I/R mechanisms responsible for progressive damage to the retina. In this study, we used a mouse model of I/R and characterized the pathogenesis by analyzing temporal changes of retinal morphology and function associated with changes in retinal gene expression. Transient ischemia was induced in one eye of C57BL/6 mice by raising intraocular pressure to 120 mmHg for 60 min
Because of a huge amount of Zn2+ in secretory granules of pancreatic islet beta-cells, Zn2+ released in certain conditions might affect the function or survival of islet cells. We studied potential paracrine effects of endogenous Zn2+ on beta-cell death. Zn2+ induced insulinoma/islet cell death in a dose-dependent manner. Chelation of released endogenous Zn2+ by CaEDTA significantly decreased streptozotocin (STZ)-induced islet cell death in an in vitro culture system simulating in vivo circumsta
Our results demonstrate the important role the JNK pathway plays in retinal degeneration in both in vitro and in vivo models and suggest that JNK inhibitors may be a useful therapeutic strategy for neuroprotection of RGCs in the retina.
Smoking cessation within 3 years may be a higher risk factor for incident metabolic syndrome than sustained smoking, indicating that weight control in ex-smokers is critical to attenuate the additional risk for incident metabolic syndrome.
Our results indicate that the presence and the degree of NAFLD are associated with arterial stiffness in nonhypertensive, nondiabetic individuals, especially in those individuals without MetS.
Continuous drinking, especially moderate-to-heavy drinking, is associated with developing MetS in Korean men, suggesting that they should be advised to restrict their alcohol consumption to <15g/day to attenuate the risk for MetS. (Circ J 2012; 76: 2363-2371).
This large observational study showed that cotinine-verified current smoking and unobserved smoking were inversely associated with hypertension in Korean adults, especially only in men.
<b>:</b> No study has reported the relationship between secondhand smoke (SHS) exposure and hypertension in self-reported never-smokers verified by nicotine metabolite. The aim of this study is to determine the relationship between SHS exposure and hypertension in self-reported and cotinine-verified never-smokers. A total of 106,268 self-reported never-smokers, verified as nonsmokers by urinary cotinine, who participated in Kangbuk Samsung Cohort study (KSCS) between 2012 and 2016 were included.
Subjects with high normal BP have greater risk factors for cardiovascular disease, including microalbuminuria, than those with normal BP. Further investigations are needed to ascertain whether more positive treatment strategies for the early prevention of cardiovascular disease might be needed for individuals with high normal BP.
These findings demonstrate epidemiologic evidence for an independent association between arterial stiffness and microalbuminuria, indices of subclinical target organ damage in nonhypertensive, nondiabetic individuals, which suggests the possibility of a similar pathophysiologic mechanism involved in these two indices of subclinical target organ damage.
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