The advancements in the molecular pathogenesis and a deeper comprehension of
cellular mechanisms of liver fibrosis promise to give new therapeutic approaches to the
management of this disease in the future.
Apoptosis, cytokines, oxidants, and inflammosomes play a complex role in favouring or
delaying the onset of liver fibrosis; sustained hepatic stellate cell activation and
transformation, without forgetting the role of hepatocytes and other complex molecular and
cellular mechanisms, are the direction that guides to fibrosis.
Therefore, in this review, after considering the causes of the development of fibrosis as
well as the interrelation between molecular and cellular profibrotic mechanisms, we will
focus on the part played in counteracting both of these actions by some anti-oxidants and
anti-fibrotic molecules such as cytokines, prostacyclin and others.
Further validation in animal studies and confirmation in clinical trials are requested. Some
data that are already available from in vitro and animal studies demonstrating the
effectiveness of novel approaches to inhibiting or treating liver fibrosis can only offer
moderate hope.
Keywords: Adiponectin, antifibrotic drugs, apoptosis, curcumine, cytokines,
extracellular matrix, gene therapy, growth factors, hepatic stellate cells, inhibitors
of metalloproteinases, interferon, liver fibrosis, metalloproteinases, N-acetyl-Lcysteine,
peroxisome proliferator-activated receptors, prostacyclin, reactive
oxygen species, relaxin, thiazolidinediones, transcription factors.
