박용환 교수
Yonghwan Park
성균관대학교 의학과 · 의학
연구실 소개
박용환 교수의 연구실은 심혈관계 질환, 특히 관상동맥 우회술 후 항혈전 요법의 최적화와 복잡한 관상동맥 병변에서의 영상 유도 시술 전략에 중점을 두고 있습니다. 또한 고유의 면역 반응 이상으로 인한 자가면역성 염증질환의 분자 기전, 특히 NLRP3 인플라마좀과 프로스타글란딘 등 염증 조절 분자의 역할을 규명하고 있습니다. 최근에는 청각 손실과 연관된 새로운 유전성 자가면역질환의 메커니즘과 IL-18 기반 염증 경로의 기전을 밝혀내는 데에도 기여하고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
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
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