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논문 기본 정보

자료유형
학술저널
저자정보
Naoshi Odagiri (Department of Hepatology Graduate School of Medicine Osaka City University) Tsutomu Matsubara (Department of Anatomy and Regenerative Biology Graduate School of Medicine Osaka City University) Misako Sato-Matsubara (Department of Hepatology Graduate School of Medicine Osaka City University) Hideki Fujii (Department of Premier Preventive Medicine Graduate School of Medicine Osaka City University) Masaru Enomoto (Department of Hepatology Graduate School of Medicine Osaka City University) Norifumi Kawada (Department of Hepatology Graduate School of Medicine Osaka City University)
저널정보
대한간학회 Clinical and Molecular Hepatology Clinical and Molecular Hepatology 제27권 제3호
발행연도
2021.1
수록면
413 - 424 (12page)

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Liver fibrosis reflects tissue scarring in the liver due to the accumulation of excessive extracellular matrix in response to chronically persistent liver injury. Hepatocyte cell death can trigger capillarization of liver sinusoidal endothelial cells, stimulation of immune cells including macrophages and Kupffer cells, and activation of hepatic stellate cells (HSCs), resulting in progression of liver fibrosis. Liver cirrhosis is the terminal state of liver fibrosis and is associated with severe complications, such as liver failure, portal hypertension, and liver cancer. Nevertheless, effective therapy for cirrhosis has not yet been established, and liver transplantation is the only radical treatment for severe cases. Studies investigating HSC activation and regulation of collagen production in the liver have made breakthroughs in recent decades that have advanced the knowledge regarding liver fibrosis pathophysiology. In this review, we summarize molecular mechanisms of liver fibrosis and discuss the development of novel anti-fibrotic therapies.

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