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The study by Ikenaga et al1 represents a significant step forward in the understanding and in the treatment approaches of hepatic fibrosis. Fibrosis is a general repair mechanism of tissue injury resulting from increased extracellular matrix (ECM) synthesis and deposition, followed by contraction of the scar, remodelling and degradation of the ECM when the tissue defect is covered and bridged. In chronic liver injury, this important protective process is altered to a morbid situation with excessive ECM accumulation, which maintains inflammation and contributes to the progression to cirrhosis and which in turn is associated with high morbidity and mortality.
Remodelling of ECM in fibrosis and cirrhosis is important for the regression of fibrosis, but also for its progression. Remodelling might even predict progression of fibrosis.2 ,3 In this context, collagen crosslinking is a key process that increases the persistence of fibrosis, in which lysyl oxidase/lysyl oxidase-like protein (LOX/LOXL) family members are crucial. The LOX/lysyl oxidase-like protein-2 (LOXL2) family is characterised by highly conserved C-terminal lysyl oxidase domain integrated by the …
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