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RISS 인기검색어
- 검색키워드
- 저자 : ( Hidekazu Tsukamoto ) (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
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Novel Drivers for Alcoholic Hepatitis and Alcohol-Promoter Liver Cancer
( Hidekazu Tsukamoto ) 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Most devastating sequela of alcoholic liver disease (ALD) are alcoholic cirrhosis, alcoholic hepatitis (AH), and liver cancer which collectively cause more than half million deaths annually in the world. As current therapeutic options are severely limited, identification of new therapeutic targets is urgently needed. Our integrated “omic” analyses of liver tissues from clinically relevant animal models and patients identify CASPASE11/4 (CASP11/4) and GASDERMIN-D (GSDMD) as novel drivers for a transition from chronic alcoholic steatohepatitis (cASH) to AH. This CASP11/4-GSD MD pathway is activated by translocated bacteria and responsible for programmed lytic cell death called pyroptosis of hepatocytes and hepatic macrophages, local dissemination of bacteria, PAMPs and DAMPs, and intense neutro philic infiltration, a hallmark of AH. Genetic suppression of this pathway, abrogates liver bacterial load, hepatocyte death, and neutrophilic infiltration and improves the liver. Conversely, genetic upregulation of the pathway, worsens AH. If this pyroptotic pathway activation is excessive, endotoxemia and septicemia may ensue leading to systemic inflammatory response syndrome (SIRS), the major complication of AH. Alcohol and Western diet synergistically promote liver tumorigenesis but the mechanisms underlying this effect is elusive. Our study discloses a novel Wnt positive loop facilitated by stearoyl co-A desaturase (SCD) in activated hepatic stellate cells (aHSCs), which links liver fibrosis to liver tumorigenesis and drives tumor promotion by alcohol and Western diet via lipid metabolic reprogram ming. Selective genetic ablation of Scd in aHSCs reduces tumor-promoting lipid metabolites in tumor microenviron ment and abrogates tumor progression. Translational relevance of this finding will be discussed.
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Satoka Aizawa,Gurmehr Brar,Hidekazu Tsukamoto 거트앤리버 소화기연관학회협의회 2020 Gut and Liver Vol.14 No.1
Cell death is now reclassified into several types based on the mechanisms and morphologic phenotype. Understanding of such classifications offers insights into the pathogenesis of liver disease, as well as diagnostic or therapeutic implications. Apoptosis is recognized relatively easily due to its unique morphology, but lytic cell death may occur in the form of accidental necrosis, mitochondria permeability transition-driven necrosis, necroptosis, pyroptosis, ferroptosis, and parthanatos. The cell may be engulfed by neighboring cells due to a loss of integrin signaling or cancer cell competition by entosis, a type of cell death. The classification also includes mechanistically termed cell death such as autophagy-dependent cell death and lysosome-dependent cell death. These different types of cell death may occur uniquely in certain liver diseases but may coexist in the evolution of the disease. They occur in parenchymal and non-parenchymal liver cells, as well as inflammatory cells, causing distinct pathologic consequences. This review briefly covers the recently revised classifications of cell death and discusses their relevance to liver diseases of different etiologies.
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