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IL-13 and TGF-β1: Core Mediators of Fibrosis

  • Cytokines That Affect Liver Fibrosis and Activation of Hepatic Myofibroblasts (Tatiana Kisseleva, Section Editor)
  • Published:
Current Pathobiology Reports

Abstract

Normal wound repair is a complex and highly orchestrated process that allows the restoration of tissue homeostasis after injury. However, when the injury is sustained, the wound-healing response becomes dysregulated leading to fibrosis. Fibrosis can affect any organ, and it is estimated that 45 % of deaths in the western world are attributed to diseases where fibrosis plays a major pathogenic role. Fibrosis is an extremely complex process that requires numerous cell types and a range of cellular processes including proliferation, differentiation, apoptosis/necrosis, ingress/egress, to name but a few. These key cellular events are controlled by a plethora of cytokines, chemokines, and growth factors including TGF-β1 and IL-13, which have been identified as critical pro-fibrotic mediators in many studies. This review will focus on the roles of TGF-β1 and IL-13 in liver fibrosis and discuss the current state of the art for therapeutic targets for these proteins and their receptors.

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Acknowledgments

We would like to express our sincere appreciation and thanks to all of our colleagues, both past and present, for their guidance and support. LAB is supported by a Newcastle University Research Fellowship. TAW is supported by the Intramural Research Program of the NIH/NIAID.

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Correspondence to Lee A. Borthwick.

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This article is part of the Topical Collection on Cytokines That Affect Liver Fibrosis and Activation of Hepatic Myofibroblasts.

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Borthwick, L.A., Wynn, T.A. IL-13 and TGF-β1: Core Mediators of Fibrosis. Curr Pathobiol Rep 3, 273–282 (2015). https://doi.org/10.1007/s40139-015-0091-1

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