Kyoto University · 의학
Etsuro Hatano 교수의 연구실은 간세포의 사멸 기전, 특히 사망수용체 유도(apoptosis)와 프로그래밍된 낭종사멸(necroptosis)의 분자 기전을 중심으로 간손상 및 간부전의 병태생리학을 규명하고 있습니다. TNF-알파 및 Fas 경로를 통한 간세포 사멸과 NF-kappa B, PI3K/Akt 경로 등 세포 생존 신호의 상호작용에 대한 기초 연구를 진행하며, 간염, 간부전, 간암 등 다양한 간질환의 치료 전략 개발에 기여하고 있습니다. 특히 약물성 간손상(예: 아세트아미노펜 중독)과 이식 후 간손상(HAT)의 분자 기전에 대한 심층적 연구도 수행하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Excessive acetaminophen (APAP) use is one of the most common causes of acute liver failure. Various types of cell death in the damaged liver are linked to APAP-induced hepatotoxicity, and, of these, necrotic cell death of hepatocytes has been shown to be involved in disease pathogenesis. Until recently, necrosis was commonly considered to be a random and unregulated form of cell death; however, recent studies have identified a previously unknown form of programmed necrosis called receptor-intera
Tumor necrosis factor-alpha receptor 1 and Fas recruit overlapping signaling pathways. To clarify the differences between tumor necrosis factor alpha (TNFalpha) and Fas pathways in hepatocyte apoptosis, primary mouse hepatocytes were treated with TNFalpha or an agonist anti-Fas antibody after infection with an adenovirus expressing an IkappaB superrepressor (Ad5IkappaB). Treatment with TNFalpha induced apoptosis in Ad5IkappaB-infected mouse hepatocytes, as we previously reported for rat hepatocy
To determine the role of phosphatidylinositol 3-kinase (PI3K)/Akt and nuclear factor-kappa B (NF-kappa B) in protecting hepatocytes from tumor necrosis factor-alpha (TNF-alpha)- and Fas-mediated apoptosis, we pretreated primary cultures of mouse hepatocytes with pharmacological and adenovirus-mediated inhibitors of the PI3K/Akt and NF-kappa B pathways followed by treatment with TNF-alpha or Jo2, an anti-Fas antibody. Jo2 and, to a lesser extent, TNF-alpha phosphorylate Akt. The PI3K inhibitor LY
Although microsurgical techniques can minimize the surgical risk factors for HAT, overtransfusion of fresh-frozen plasma in high-risk patients (ABO incompatible) may be a critical factor in the development of HAT in LRLT.
The SUV ratio was related significantly to disease-related death as well as other predictive factors, including the number of tumors, the size, stage, and involvement of vessels, and the involvement of the capsule. Consequently, we conclude that the SUV ratio provides information of prognostic relevance in patients with HCC before surgery.
Death receptor-mediated hepatocyte apoptosis is implicated in a wide range of liver diseases including viral hepatitis, alcoholic hepatitis, ischemia/reperfusion injury, fulminant hepatic failure, cholestatic liver injury, and cancer. Our aim was to clarify the protective pathway in death receptor-mediated hepatocyte apoptosis and the significance of apoptosis in liver injury. In vitro: AdIkappaBsr plus tumor necrosis factor (TNF)-alpha/Jo2 rapidly induced apoptosis in mouse hepatocyte, whereas
Administration of SP600125 to DEN-treated rats shifted hepatocytic Smad3-mediated signal from oncogenesis to tumor suppression, thus suggesting that JNK could be a therapeutic target of human HCC development and progression.
