Special Issue "Liver Damage and Repair"
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (31 March 2019)
Prof. Dr. Giuliano Ramadori
Department of Internal Medicine, Gastroenterology/Endocrinology,University of Gottingen, Germany
The liver is a “frontier” organ located between two different “worlds”. The first world is the “external world”, which comprises all the nutrients necessary for normal growth and functioning of the body, on the other hand, potentially dangerous components, such as excess of calorie intake, alcoholic beverages, bacteria, bacterial components, viruses, xenobiotics, etc., introduced daily into the body via food through the alimentary tract. The second world is the “internal world” which depends on the delivery of energy sources, hormones and minerals to keep the body functioning under normal and under “emergency” conditions. Under normal conditions, the liver(hepatocyte) takes up the elements from the nutrients absorbed through the small intestine and the waste (Kupffer cells) from the large intestine, both reaching the liver through the portal blood. From the arterial blood of the systemic circulation, the liver takes up xenobiotics (hepatocytes) and “waste” material such as aged erythrocytes, corpuscolate matters and microorganisms reaching systemic circulation trough the blood (Kupffer cells) and hormones from the adrenal glands, thyroid and from the hypophysis (hepatocyte). The most important cells physiologically involved in liver function are the hepatocyte and the liver macrophage, the Kupffer cell. Although the functional “plasticity” of the liver is such that it can clear large amounts of noxious material, when the quality or quantity of the “waste” overcomes the intracellular defense mechanisms it can lead to recruitment of inflammatory cells and to hepatocellular damage.
The damaged cells are then cleared by the mononuclear phagocytes and restitutio ad integrum takes place. In cases of continuous exposure of the liver to the noxious agents and to the inflammatory cells replacement of the damaged cells with healthy ones is no more possible and structural tissue changes become necessary. Liver fibrosis progresses to cirrhosis. As a consequence, hepatic blood supply switches from the mainly portal blood to arterial blood from the hepatic artery. This leads to the so called capillarisation of the sinusoids in the “restructured” remaining liver tissue. Portal blood then reaches the vena cava through collateral vessels of the portal vein, which develop into true varices in the lower esophagus and stomach.
If the noxious agent(s) is eliminated however, a reversible stage can follow. If not, cirrhosis can further progress to an irreversible shrinkage of the organ. Functional activity is then strongly reduced to a minimum(rest) which is provided by the maximally engaged remaining parenchymal and non-parenchymal cells. This functional capacity can be further reduced by the persistence of inflammatory infiltrate and ongoing cellular damage. Under this condition the risk of cancer development reaches 5-8%/year and decompensation symptoms become apparent.
- Cellular pathology in acute and chronic liver damage of different origin in human liver
- Nutrition and the liver: how can we decide alcoholic, non-alcoholic?
- Iron, copper and the liver
- The liver and the endocrine system in health and disease
- Hepatotropic viruses and liver diseases: Clinics and liver pathology
- Liver and radiobiology: just another damaging agent?
- Intracellular defense mechanisms in liver cells (hepatocyte, Kupffer cell)
- Mechanisms of inflammation in acute and in “chronic” liver damage
- Mechanisms of damage and repair: Ischemia-ripe fusion injury
- Fibrosis, cirrhosis: mechanisms of development and clinical consequences
- How can we stop fibrosis development and when does it make sense?
- Tumor development: What is special in the liver?
Prof. Dr. Giuliano Ramadori
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