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Commentary
Selective LOXL2 inhibition: potent antifibrotic effects in ongoing fibrosis and fibrosis regression
  1. Fernando Magdaleno1,2,
  2. Jonel Trebicka1,3,4
  1. 1Department of Internal Medicine I, University of Bonn, Bonn, Germany
  2. 2Department of Pathology, University of Illinois at Chicago, Chicago, Illinois, USA
  3. 3Institute of Clinical Research, Odense University Hospital, University of Southern Denmark, Odense, Denmark
  4. 4European Foundation for the Study of Chronic Liver Failure, Travessera de Gràcia, Barcelona, Spain
  1. Correspondence to Professor Jonel Trebicka, European Foundation for the Study of Chronic Liver Failure, Travessera de Gràcia, 11, 7th floor, Barcelona 08021, Spain; jonel.trebicka{at}efclif.com

https://doi.org/10.1136/gutjnl-2016-313621

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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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    Footnotes

    • Contributors FM and JT reviewed the literature and wrote the commentary.

    • Funding JT is supported by grants from the Deutsche Forschungsgemeinschaft (SFB TRR57 P18), European Union H2020 and Cellex Foundation.

    • Competing interests None declared.

    • Provenance and peer review Commissioned; internally peer reviewed.

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