Keio University · 의학
Koichi Fukunaga 교수의 연구실은 호흡기 질환, 특히 급성 폐손상(Acute Lung Injury)의 병태생리학적 기전과 자가 회복 메커니즘을 중심으로 연구를 진행하고 있습니다. 특히 폐 손상 이후 복구를 촉진하는 내재적 생리적 메커니즘, 예를 들어 COX-2 유도 및 생활소재 지질(예: presqualene diphosphate)의 대사 조절을 통해 염증 반응의 종결을 규명하고자 합니다. 이는 전통적인 항염증 치료 접근과는 다른, 회복 촉진 기반의 새로운 치료 전략 개발을 목표로 하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Acute lung injury (ALI) is a severe illness with excess mortality and no specific therapy. In its early exudative phase, neutrophil activation and accumulation in the lung lead to hypoxemia, widespread tissue damage, and respiratory failure. In clinical trials, inhibition of proinflammatory mediators has not proven effective. In this study, we pursued a new investigative strategy that emphasizes mediators promoting resolution from lung injury. A new spontaneously resolving experimental murine mo
Host genetics is a key determinant of COVID-19 outcomes. Previously, the COVID-19 Host Genetics Initiative genome-wide association study used common variants to identify multiple loci associated with COVID-19 outcomes. However, variants with the largest impact on COVID-19 outcomes are expected to be rare in the population. Hence, studying rare variants may provide additional insights into disease susceptibility and pathogenesis, thereby informing therapeutics development. Here, we combined whole
Presqualene diphosphate (PSDP) is a bioactive lipid that rapidly remodels to presqualene monophosphate (PSMP) upon cell activation (Levy, B. D., Petasis, N. A., and Serhan, C. N. (1997) Nature 389, 985-990). Here, we have identified and characterized a phosphatase that converts PSDP to PSMP. Unlike the related polyisoprenyl phosphate farnesyl diphosphate (FDP), PSDP was not a substrate for type 2 lipid phosphate phosphohydrolases. PSDP phosphatase activity was identified in activated human neutr
