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Targeting Focal Adhesion Kinase in Fibrotic Diseases

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Abstract

Fibrotic diseases such as idiopathic pulmonary fibrosis or scleroderma (systemic sclerosis) are chronic fibroproliferative disorders for which there are currently no effective treatments. Dysregulated normal tissue repair process is considered to cause a fibrotic response culminating in compromised organ function due to excess extracellular matrix deposition. The mechanisms underlying the pathophysiology of fibrosis are poorly understood. Recent findings suggest that focal adhesion kinase (FAK) plays a key role in development of fibrotic disorders, and it appears to be an attractive target for antifibrotic therapy. Here, we review the emerging role of FAK as a key regulator of fibrotic signaling and its potential as a future therapeutic target to counteract fibrosis.

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Notes

  1. Smad family member 3: the SMAD proteins are homologs of both the Drosophila protein, mothers against decapentaplegic (MAD) and the Caenorhabditis elegans protein SMA (from gene sma for small body size).

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Authors and Affiliations

  1. Department of Medicine, Pulmonary and Critical Care Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA

    David Lagares

  2. Department of Medicine, University of Montreal, 1560 Sherbrooke Street East, Pavillon DeSève, Room Y2621, Montreal, QC, H2L 4M1, Canada

    Mohit Kapoor

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Lagares, D., Kapoor, M. Targeting Focal Adhesion Kinase in Fibrotic Diseases. BioDrugs 27, 15–23 (2013). https://doi.org/10.1007/s40259-012-0003-4

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