Complex molecular and cellular mechanisms are involved in the pathway of liver fibrosis. Activation and
transformation of hepatic stellate cells (HSCs) are considered the two main reasons for the cause and development of liver
fibrosis. The peroxisome proliferator-activated receptors (PPARs) belonging to the family of ligand-activated transcription
factors play a key role in liver homeostasis, regulating adipogenesis and inhibiting fibrogenesis in HSCs. Normal
transcriptional function of PPARs contributes to maintain HSCs in quiescent phase. A reduced expression of PPARs in
HSCs greatly induces a progression of liver fibrosis and an increased production of collagen. Here, we discuss role and
function of PPARs and we take into consideration molecular factors able to reduce PPARs activity in HSCs. Finally, although
further validations are needed, we illustrate novel strategies available from in vitro and animal studies on how
some PPARs-agonists have been proved effective as antifibrotic substances in liver disease.
Keywords: Cytokines, genes, HSCs, ligands, liver fibrosis, microcirculation, PPARs, antifbrotic therapy, transcription factors.
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