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Abstract
Models of liver fibrosis, which include cell culture models, explanted and biopsied human material, and experimental animal models, have demonstrated that liver fibrosis is a highly dynamic example of solid organ wound healing. Recent work in human and animal models has shown that liver fibrosis is potentially reversible and, in specific circumstances, demonstrates resolution with a restoration of near normal architecture. This Review highlights the manner in which studies of models of liver fibrosis have contributed to the paradigm of dynamic wound healing in this solid organ.
Authors
John P. Iredale
Figure 1
Sinusoidal events in the development of liver fibrosis.
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Injury to hepatocytes results in the recruitment and stimulation of inflammatory cells, as well as the stimulation of resident inflammatory cells (including Kupffer cells). Factors released by these inflammatory cells lead to transformation of HSCs into a myofibroblast-like phenotype. HSC activation leads to accumulation of scar (fibrillar) ECM. The presence of a fibrillar ECM in the Disse space has consequences for hepatocyte function, leading to the loss of microvilli and endothelial fenestrae. Therefore, the loss of normal tissue architecture contributes to impairment of organ function. Figure modified with permission from Journal of Biological Chemistry (119 ).
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ISSN: 0021-9738 (print), 1558-8238 (online)