**7. References**


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**Acknowledgement** 

compounds he has provided.

Cells. Moscow: Nauka, 208 p.

We are sincerely grateful to the Chair of the Petrozavodsk State University Molecular Biology Department (Russia), DSc, Professor N. N. Nemova for her invaluable help in the preparation of the manuscript. Special thanks are due also to Professor V. P. Andreev of the St. Petersburg State University Organic Chemistry Department (Russia) for the chemical

The study was supported by the Government of the Russian Federation grant № 11.G34.31.0052 (Ordinance 220), and RF Presidential grant for leading scientific schools №

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**Chapter 8** 

© 2012 Tsuji and Oguchi, licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2012 Tsuji and Oguchi, licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

alcoholic liver injury in which we carried out some investigations [12-15].

**Some Findings on Apoptosis in Hepatocytes** 

For development of novel strategy for the treatment of hepatic diseases, in which changes in apoptosis are targeted, it is most important to understand the molecular mechanisms by which apoptotic process is regulated. Rapid and efficient removal of unwanted cells such as aged, damaged, genetically mutated, or virally-infected ones is indispensable in the maintenance of the health of the liver. Means for removal of such cells are provided by nature as apoptosis, a well-controlled and programmed cell death process, which is especially important in the liver where cells are exposed to various toxins and viruses [1]. In a healthy adult body, the number of cells removed by apoptotic process in a certain period of time is comparable to the number of cells that proliferate by mitosis. Proper homeostasis of organs is thus maintained. However, under certain pathophysiological conditions, the balance between the growth and the loss of the cells is often upset, due to the onset of some liver diseases resulting in the loss of tissue homeostasis. Insufficient apoptosis will promote the growth of hepatocarcinoma or biliary carcinoma by failing the removal of cells growing uncontrollably in genetically mutated cells or in chronic or persistent inflammations [2-5]. Persistent stimulation causing apoptosis may be a factor to promote high rate regeneration of cancer cells in the tissue, elevating the risk of errors in mitosis. In contrast, excessive and/or persistent apoptosis may lead to acute damages such as fulminant hepatitis or reperfusion injury [6, 7], or chronic persistent damages such as alcoholic liver diseases, cholestatic liver disease, or viral hepatitis [8-11]. Inhibition of apoptosis in the liver injury or selective killing of malignant cells in tumors will provide strategies for treatment of hepatic diseases. In fact, new drug development is ongoing targeting apoptosis through the understanding of molecular process and pathophysiological role of apoptosis, and such substances are now tested in clinical trial or used as new options for certain human diseases. In this review, we focus the subject on the role of apoptosis in cholestatic liver diseases or

Mayumi Tsuji and Katsuji Oguchi

http://dx.doi.org/10.5772/51015

**1. Introduction** 

Additional information is available at the end of the chapter

