الفهرس 
Anatomy and morphology of the liverOnly 14 pages are availabe for public view
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Abstract
The final event of chronic liver injury, independently from the aetiological agent, is hepatic fibrosis. It is characterized by
excessive extracellular matrix (ECM)deposition that distorts the
hepatic architecture by forming fibrotic scars, and the
subsequent development of nodules of regenerating hepatocytes
this defines liver cirrhosis which leads to liver cell failure.
Hepatic fibrosis was historically thought to be a passive
phenomenon because of the collapse of the hepatic parenchyma
following necrosis but currently, hepatic fibrosis is considered a
model of the wound-healing response to chronic liver injury .
Activation of hepatic stellate cells (HSCs), leading to
accumulation of extracellular matrix, is the central event of
fibrogenesis.
Exciting progress has been made in understanding the
molecular basis of this process.
1) The effects (and signalling pathways) of key cytokines
on HSCs.
2) understanding the transcriptional regulation following
HSC activation.
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3) characterisation of matrix proteases and their inhibitors
4) demonstration of apoptosis as an important event in the
resolution of hepatic fibrosis, and identification of its mediators.
5) understanding the role of other cellular elements in
hepatic fibrosis and their interaction with HSCs.
Growing understanding of the pathogenesis of hepatic
fibrosis indicates potentially powerful noninvasive (blood)
biomarkers of hepatic fibrogenesis and fibrosis which can be
sub-divided in two classes: Class I fibrosis biomarkers are
pathophysiologically derived from ECM turnover and/or from
changes of the fibrogenic cell types in liver. These biomarkers
do not indicate the extent of connective tissue deposition, that
is, the stage of fibrotic transition of the organ In contrast, class
II fibrosis markers have been statistically proven (multi-variate
analyses) to be best correlated with fibrosis and to a lesser
extent with fibrogenesis or fibrolysis. Class II markers mostly
estimatethe degree of the fibrosis .
There is no standard treatment for liver fibrosis. Although
obvious in principle, it is important to emphasize that the most
effective antifibrotic therapies are likely to remove the
underlying stimulus to fibrogenesis. For example eradication or
inhibition of hepatitis B virus or hepatitis C virus (HCV) leads
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to reversion of fibrosis, even in some patients with histologic
cirrhosis .
There is other new abroaches for the treatment of hepatic
fibrosis either by:
1) Anti inflammatories suppressing the infilamatory response to
the injuirous aggents.
2) Moddulation of the immune response of the liver tissue.
3) Downregulation of hepatic stellate cells activations.