Liver Diseases: From Molecular Basis to Potential Therapy

Dear Colleagues,

The liver is the largest organ of the body. Anatomically, it is located between the gastrointestinal tract and the systemic circulation. The liver is not only essential for the digestion of food stuffs introduced through the mouth and for the elimination of ingested toxicants and particulate matter which reaches the portal blood on the other side, but it also satisfies the need of such nutrients by distributing them to the rest of the body. A crucial function is the elimination of old erythrocytes and the delivery of the necessary components for replacement of the blood cells to the bone marrow. By producing the bulk of the plasma proteins, first albumin, but also those of the coagulation and complement system the liver is responsible for the corpuscolate and fluid components of the blood. Those proteins fulfill essential functions under normal, but more importantly under dangerous conditions, when the integrity of the liver itself, or more often when the integrity of extrahepatic tissues, is compromised. The Encyclopedia Britannica defines “disease, any harmful deviation from the normal structural or functional state of an organism, generally associated with certain signs and symptoms and differing in nature from physical injury”. The normal condition of the liver is still not well defined at the molecular level. This is, however, essential in order to recognize a disease as the consequence of the interruption of the different functions. A demarcation between disease and health may not always be apparent as the liver has a large functional reserve. This can, however, be overwhelmed in cases such as drug-induced liver damage, irradiation-induced liver fat accumulation, and acute or long-term damage or in some complications of pregnancy.

Topics of interest:

1. Quality and quantity of lipids in different forms of steatosis in lean overweight and obese persons;
2. Molecular consequences of lipids accumulation in the hepatocytes, e.g., bile production, protein synthesis including chemokines and cytokines;
3. Mechanisms of hepatocellular damage induced by lipid accumulation;
4. Consequences of steatosis for blood cell formation in the bone marrow;
5. Consequences of steatosis for DNA-synthesis in hepatocellular nuclei;
6. Ameiosis in the liver;
7. Lipid overloading and mechanisms of volume change of the liver;
8. Consequences of lipid overloading for extracellular matrix production and deposition;
9. Liver and pregnancy: pathophysiology of HELLP-syndrome (coagulation, complement, production of blood cells);
10. Molecular mechanisms of acute fatty liver and pregnancy;
11. Molecular mechanisms of cholestatic disease in pregnancy;
12. Irradiation effect on the liver and on liver cells;
13. Irradiation and intracellular molecular changes;
14. How can irradiation induce liver damage by regulating chemokine and cytokine-production.

Prof. Dr. Giuliano Ramadori
Guest Editor

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