Yonghwan Park
Sungkyunkwan University · 医学
研究室紹介
Professor Yonghwan Park's research lab focuses on the pathogenesis of autoinflammatory diseases, particularly those driven by dysregulation of the innate immune system, with a strong emphasis on inflammasome activation and cytokine signaling (e.g., IL-1β and IL-18). The lab investigates genetic mutations in key immune regulators such as OTULIN and Wdr1, linking them to systemic inflammation and tissue-specific manifestations like hearing loss and skin disease. Using translational approaches, including patient-derived cells and mouse models, the lab explores the role of lipid mediators like PGE2 in modulating inflammasome activity and immune homeostasis. The work also extends to interventional cardiology, examining optimal antiplatelet strategies post-percutaneous coronary intervention.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Importance: Data on P2Y12 inhibitor monotherapy after short-duration dual antiplatelet therapy (DAPT) in patients undergoing percutaneous coronary intervention are limited. Objective: To determine whether P2Y12 inhibitor monotherapy after 3 months of DAPT is noninferior to 12 months of DAPT in patients undergoing PCI. Design, Setting, and Participants: The SMART-CHOICE trial was an open-label, noninferiority, randomized study that was conducted in 33 hospitals in Korea and included 2993 patients
Among patients with complex coronary-artery lesions, intravascular imaging-guided PCI led to a lower risk of a composite of death from cardiac causes, target-vessel-related myocardial infarction, or clinically driven target-vessel revascularization than angiography-guided PCI. (Supported by Abbott Vascular and Boston Scientific; RENOVATE-COMPLEX-PCI ClinicalTrials.gov number, NCT03381872).
Systemic autoinflammatory diseases are caused by mutations in genes that function in innate immunity. Here, we report an autoinflammatory disease caused by loss-of-function mutations in OTULIN (FAM105B), encoding a deubiquitinase with linear linkage specificity. We identified two missense and one frameshift mutations in one Pakistani and two Turkish families with four affected patients. Patients presented with neonatal-onset fever, neutrophilic dermatitis/panniculitis, and failure to thrive, but
PGE2 is a potent lipid mediator involved in maintaining homeostasis but also promotion of acute inflammation or immune suppression in chronic inflammation and cancer. Nucleotide-binding domain, leucine-rich repeat-containing protein (NLR)P3 inflammasome plays an important role in host defense. Uncontrolled activation of the NLRP3 inflammasome, owing to mutations in the NLRP3 gene, causes cryopyrin-associated periodic syndromes. In this study, we showed that NLRP3 inflammasome activation is inhib
causes autosomal-dominant sensorineural hearing loss in two unrelated families. In family LMG446, hearing loss is accompanied by autoinflammatory signs and symptoms without serologic evidence of inflammation as part of an atypical CAPS phenotype and was reversed or improved by IL-1β blockade therapy. In family LMG113, hearing loss segregates without any other target-organ manifestations of CAPS. This observation led us to explore the possibility that resident macrophage/monocyte-like cells in th
Gain-of-function mutations that activate the innate immune system can cause systemic autoinflammatory diseases associated with increased IL-1β production. This cytokine is activated identically to IL-18 by an intracellular protein complex known as the inflammasome; however, IL-18 has not yet been specifically implicated in the pathogenesis of hereditary autoinflammatory disorders. We have now identified an autoinflammatory disease in mice driven by IL-18, but not IL-1β, resulting from an inactiv
Despite recent successful efforts to shorten the door-to-balloon time in patients with acute ST-segment elevation myocardial infarction (STEMI), prehospital delay remains unaffected. Nonetheless, the factors associated with prehospital delay have not been clearly identified in Korea. We retrospectively evaluated 423 patients with STEMI. The mean symptom onset-to-door time was 255 ± 285 (median: 150) min. The patients were analyzed in two groups according to symptom onset-to-door time (short dela
Despite recent successful efforts to shorten the door-to-balloon time in patients with acute ST-segment elevation myocardial infarction (STEMI), prehospital delay remains unaffected. Nonetheless, the factors associated with prehospital delay have not been clearly identified in Korea. We retrospectively evaluated 423 patients with STEMI. The mean symptom onset-to-door time was 255 ± 285 (median: 150) min. The patients were analyzed in two groups according to symptom onset-to-door time (short dela