Can Your Liver Regenerate If You Have Cirrhosis?
In recent years, there has been great interest in the possibility of obtaining regression of hepatic fibrosis, taking into account the results achieved with the treatment of chronic hepatitis C virus. However, at present there is controversy over the meaning of the terms reversion and regression of fibrosis liver cirrhosis. Reversal of cirrhosis implies complete restoration of the liver architecture until normality, with disappearance of it; instead, regression consists of “improvement” of fibrosis/cirrhosis to a lower degree than initially found arriving in some cases to normality.
The possibility of stopping or disappearing fibrosis/cirrhosis constitutes an important research focus of the latter decades that challenges the “old” conception of the irreversibility of hepatic fibrosis, considered a unidirectional alteration without the possibility of being returned.
Liver fibrosis is considered an answer for healing, which is meant to limit the tissue damage produced by chronic liver damage independently of the etiology, but when the aggression is persistent, this healing process can produce alteration of the hepatic architecture due to the appearance of cirrhosis, which is characterized by bands of fibrosis, parenchymatous regeneration nodules and vascular distortion.
The composition of the hepatic fibrous scar is similar, regardless of the cause of the injury, either of viral origin (hepatitis B or C virus), drugs, alcohol, autoimmune or metabolic diseases (Hemochromatosis, Wilson…).
Fibrosis occurs at the sites of greatest injury and usually requires that the harmful stimulus persists for many months or years.
While this process had classically been considered irreversible, clinical and experimental evidence suggests on the contrary.
The review of histological samples of patients with chronic liver diseases of various etiologies successfully treated with their respective therapies, and also samples of animal models of fibrosis, indicate that fibrosis is a bidirectional and dynamic process in which recovery and remodeling can occur in the scar tissue, mainly in the initial stages. However, it is still unknown the point from which the cirrhosis does not return or is irreversible.
In order for fibrosis to start, some elements (that are derived from the injury of the hepatocytes and not necessarily from the presence of inflammatory cells) are required, as it has been demonstrated in hemochromatosis for example, in which there are no inflammatory cells.
Histologically, the liver is composed of parenchymal cells (hepatocytes) and nonparenchymal cells. Hepatocytes represent 80% of the hepatic volume and non-parenchymal cells 6.5% of the total of the liver and 40% of these are found in hepatic sinusoids, in which there are three types of cells: endothelial cells, Kupffer cells and the hepatic stellate cells.
The hepatic stellate cells are perisinusoidal cells located in the subendothelial space of the Disse space, that in their quiescent state have as their main function serve as a repository of retinoids (vitamin A and its metabolites).
However, in the face of aggressive stimuli as a virus, alcohol or others, through the process of “activation”, these cells are transformed into others totally different, morphologically similar to the myofibroblasts (they are the mesenchymal cell type responsible for wound healing and tissue repair across all organs and various physiological states) but with multiple additional functions as the production of the extracellular matrix and of proinflammatory cytokines. This myofibroblast is characterized by its proliferation, contractile activity and fibrogenesis (development of fibrous tissue). The hepatic stellate cells were identified in the 1990s as an important source of collagen within the liver and, starting of that knowledge; liver fibrosis began to receive greater attention. These cells are in physical contact with hepatocytes and with endothelial cells of the hepatic sinusoids with their cytoplasmic prolongations.
It is estimated that 85% of the vitamin A content in the liver is in the hepatic stellate cells.
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