The balancing act of the liver: tissue regeneration versus fibrosis
Lucía Cordero-Espinoza and Meritxell Huch
Wellcome Trust/CRUK Gurdon Institute, Wellcome Trust–Medical Research Council Stem Cell Institute, and Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom.
Address correspondence to: Meritxell Huch, Wellcome Trust/Cancer Research UK Gurdon Institute, Henry Wellcome Building of Cancer and Developmental Biology, Tennis Court Road, Cambridge CB2 1QN, United Kingdom. Phone: 44.0.1223.334088; Email: m.huch@gurdon.cam.ac.uk.
Find articles by Cordero-Espinoza, L. in: JCI | PubMed | Google Scholar
Wellcome Trust/CRUK Gurdon Institute, Wellcome Trust–Medical Research Council Stem Cell Institute, and Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom.
Address correspondence to: Meritxell Huch, Wellcome Trust/Cancer Research UK Gurdon Institute, Henry Wellcome Building of Cancer and Developmental Biology, Tennis Court Road, Cambridge CB2 1QN, United Kingdom. Phone: 44.0.1223.334088; Email: m.huch@gurdon.cam.ac.uk.
Find articles by Huch, M. in: JCI | PubMed | Google Scholar
First published January 2, 2018 - More info
J Clin Invest. 2018;128(1):85–96. https://doi.org/10.1172/JCI93562.
Copyright © 2018, American Society for Clinical Investigation
Epithelial cell loss alters a tissue’s optimal function and awakens evolutionarily adapted healing mechanisms to reestablish homeostasis. Although adult mammalian organs have a limited regeneration potential, the liver stands out as one remarkable exception. Following injury, the liver mounts a dynamic multicellular response wherein stromal cells are activated in situ and/or recruited from the bloodstream, the extracellular matrix (ECM) is remodeled, and epithelial cells expand to replenish their lost numbers. Chronic damage makes this response persistent instead of transient, tipping the system into an abnormal steady state known as fibrosis, in which ECM accumulates excessively and tissue function degenerates. Here we explore the cellular and molecular switches that balance hepatic regeneration and fibrosis, with a focus on uncovering avenues of disease modeling and therapeutic intervention.
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