Fate tracing reveals hepatic stellate cells as dominant contributors to liver fibrosis independent of its aetiology

Ingmar Mederacke, Christine C. Hsu, Juliane S. Troeger, Peter Huebener, Xueru Mu, Dianne H. Dapito, Jean-Philippe Pradere and Robert F. Schwabe ()
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Ingmar Mederacke: College of Physicians and Surgeons, Columbia University
Christine C. Hsu: College of Physicians and Surgeons, Columbia University
Juliane S. Troeger: College of Physicians and Surgeons, Columbia University
Peter Huebener: College of Physicians and Surgeons, Columbia University
Xueru Mu: College of Physicians and Surgeons, Columbia University
Dianne H. Dapito: Institute of Human Nutrition, Columbia University
Jean-Philippe Pradere: College of Physicians and Surgeons, Columbia University
Robert F. Schwabe: College of Physicians and Surgeons, Columbia University

Nature Communications, 2013, vol. 4, issue 1, 1-11

Abstract: Abstract Although organ fibrosis causes significant morbidity and mortality in chronic diseases, the lack of detailed knowledge about specific cellular contributors mediating fibrogenesis hampers the design of effective antifibrotic therapies. Different cellular sources, including tissue-resident and bone marrow-derived fibroblasts, pericytes and epithelial cells, have been suggested to give rise to myofibroblasts, but their relative contributions remain controversial, with profound differences between organs and different diseases. Here we employ a novel Cre-transgenic mouse that marks 99% of hepatic stellate cells (HSCs), a liver-specific pericyte population, to demonstrate that HSCs give rise to 82–96% of myofibroblasts in models of toxic, cholestatic and fatty liver disease. Moreover, we exclude that HSCs function as facultative epithelial progenitor cells in the injured liver. On the basis these findings, HSCs should be considered the primary cellular target for antifibrotic therapies across all types of liver disease.

Date: 2013
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DOI: 10.1038/ncomms3823

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