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Abstract: ATX is a secreted glycoprotein with lysophospholipase D (lysoPLD) activity, which
is the key enzyme in the production of lysophosphatidic acid (LPA). LPA is widely distributed
in various body fluids and participates in various life activities by binding to at least six
G-protein-coupled receptors (GPCR) on the cell membrane to activate various pathways.
When liver fibrosis develops, the levels of ATX and LPA in blood increase. The ATX-LPA
axis plays a central driving role in the process of liver fibrosis and is recognized as a potential
target for liver fibrosis therapy. At present, multiple ATX inhibitors have been validated in
various liver fibrosis models. This review focused on the mechanism of ATX-LPA axis in
liver fibrosis, the diagnostic and prognostic value of serum ATX levels, and the development
of ATX inhibitors to explain the pathophysiological significance of the regulation of this axis.
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