Publication: Liver fibrosis: a dynamic and potentially reversible process
Authors
Povero, Davide ; Busletta, Chiara ; Novo, Erica ; Valfrè di Bonzo, Lorenzo ; Cannito, Stefania ; Paternostro, Claudia ; Parola, Maurizio
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
In any chronic liver disease (CLDs),
whatever the aetiology, reiteration of liver injury results
in persisting inflammation and progressive fibrogenesis,
with chronic activation of the wound healing response in
CLDs, representing a major driving force for progressive
accumulation of ECM components, eventually leading to
liver cirrhosis. Cirrhosis is characterized by fibrous septa
dividing the hepatic parenchyma into regenerative
pseudo-lobules, as well as by extensive changes in
vascular architecture, the development of portal
hypertension and related complications. Liver
fibrogenesis (i.e., the dynamic process leading to
increased deposition of ECM and much more) can lead
to different patterns of fibrosis and is sustained by
myofibroblast-like cells (MFs) of different origin, with
activated hepatic stellate cells (HSC/MFs) being the
major cell type involved. Major pro-fibrogenic
mechanisms also include oxidative stress, as well as
derangement of epithelial-mesenchymal interactions
and, as recently suggested, the process of epithelial to
mesenchymal transition (EMT).
Liver fibrosis has been considered traditionally as an
irreversible process but experimental and clinical
literature data published in the last decade have
suggested that both the removal of the aetiological agent
or condition, as well as an effective therapy, can result in
significant regression of liver fibrosis. This is usually
associated, particularly in animal models, with induction
of apoptosis in MFs but, unfortunately, human HSC/MFs
are much more resistant to apoptosis than murine MFs.
However, clinical studies provided no unequivocal
evidence for a complete reversal of cirrhosis or a significant reversal of vascular changes in conditions of
established cirrhosis.
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