Woon Yong Kwon
Seoul National University · Medicine
About the Lab
Professor Woon Yong Kwon's research lab specializes in critical care and translational immunology, focusing on the molecular mechanisms underlying sepsis-induced organ injury, particularly acute lung injury and brain injury. The lab investigates protective pathways involving key molecules such as NF-κB, HSP70, HMGB-1, and mitochondrial formyl peptides, with an emphasis on therapeutic interventions using niacin, selenium, glutamine, and S1P1 modulators. Their work bridges preclinical models with clinical relevance, aiming to identify novel targets and combination therapies to improve survival and organ function in septic shock. The lab integrates in vitro cell studies with in vivo rat models of sepsis to dissect signaling pathways and evaluate therapeutic efficacy.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15High dose of niacin attenuated lung inflammation, reduced histologic lung damages, and improved survival during sepsis in rats. These therapeutic benefits were associated with downregulation of the NF-κB pathway.
Heat shock protein 70 (HSP70) is reported as the main factor responsible for the beneficial effects of glutamine (GLN) and as a negative regulator of high mobility group box protein-1 (HMGB-1) expression. Our aim was to determine whether GLN attenuates acute lung injury (ALI) by the inhibition of HMGB-1 expression during sepsis. Male Sprague-Dawley rats were subjected to caecal ligation and puncture (CLP) to induce sepsis. GLN or saline was administered through tail vein 1 h after CLP. Then, que
4F attenuated acute lung injury and improved survival in endotoxemic rats. The therapeutic benefits of 4F were found to be associated with the stimulation of S1P1, the activation of Akt, the down-regulation of the NF-κB pathway, and the suppression of cell adhesion molecules.
Significance Septic shock commonly leads to multiorgan injury both directly via tissue inflammation and secondarily via hypoperfusion, but both can result in mitochondrial N -formyl peptide (mtFP) release into the circulation. However, no studies have evaluated the role of circulating mtFPs during septic shock. We found that a relatively high plasma nicotinamide adenine dinucleotide dehydrogenase subunit-6 (the most potent human mtFP) level was independently associated with the development of se
OBJECTIVES: To determine whether the combination therapy of niacin and selenium attenuates lung injury and improves survival during sepsis in rats and whether its benefits are associated with the activation of the glutathione redox cycle and up-regulation of nuclear factor erythroid 2-related factor 2. DESIGN: Prospective laboratory study. SETTING: University laboratory. SUBJECTS: Human lung microvascular endothelial cells and male Sprague-Dawley rats (n = 291). INTERVENTION: In lipopolysacchari
Single high dose and repeated low dose of niacin attenuated brain injury and improved neurological outcome after cardiac arrest in rats. Their therapeutic benefits were associated with suppressions of the phosphorylations of p38 and c-Jun N-terminal kinase/stress-activated protein kinase and the cleavage of caspase 3.
Regardless of target temperatures, low rSO<sub>2</sub> levels during TTM were significantly associated with poor 6-month neurological outcomes in OHCA survivors.
OBJECTIVES: To determine neuroprotective effects and mechanism of the combination therapy of niacin and selenium in cardiac arrest rats. DESIGN: Prospective laboratory study. SETTING: University laboratory. SUBJECTS: Rat cortex neurons and male Sprague-Dawley rats (n = 68). INTERVENTIONS: In rat cortex neurons underwent 90 minutes of oxygen-glucose deprivation and 22.5 hours of reoxygenation, effects of the combination therapy of niacin (0.9 mM) and selenium (1.5 μM) were investigated. The role
BACKGROUND: Trauma induces neutrophil migration toward injury sites, both initiating wound healing and protecting against local bacterial infection. We have previously shown that mitochondrial formyl peptides (mtFPs) released by injured tissues act as chemoattractants by ligating neutrophil (PMN) formyl peptide receptor 1 (FPR1). But this process can also internalize multiple neutrophil chemoattractant receptors and thus might limit neutrophil migration to the lung in response to bacteria. Our o
OBJECTIVES: We performed this study to investigate the association of prehospital supraglottic airway (SGA) on neurologic outcome in cardiac arrest victims with adjustment of postresuscitation variables as well as prehospital and resuscitation variables. METHODS: This study was a retrospective study based on a multicenter prospective cohort registry from December 2013 to April 2016. According to the 28-day cerebral performance categories (CPCs) scale, patients were divided into the good-outcome
The aim of this study was to develop and evaluate a triage method to prevent unnecessary emergency department visits of out-of-hospital poisoned patients. From October 2003 to September 2004, the calls that lay persons gave to the Seoul Emergency Medical Information Center to seek advice on the out-of-hospital poisoned patients were enrolled. We designed a triage protocol that consisted of five factors and applied it to the patients. According to the medical outcomes, we classified the patients
Research Areas
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