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Andrew Leask
Researcher at University of Western Ontario
Publications - 199
Citations - 11342
Andrew Leask is an academic researcher from University of Western Ontario. The author has contributed to research in topics: CTGF & Fibrosis. The author has an hindex of 52, co-authored 191 publications receiving 10451 citations. Previous affiliations of Andrew Leask include University of Saskatchewan.
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All in the CCN family: essential matricellular signaling modulators emerge from the bunker.
Andrew Leask,David Abraham +1 more
TL;DR: The CCN family of secreted proteins not only regulate crucial biological processes including cell differentiation, proliferation, adhesion, migration, apoptosis, ECM production, chondrogenesis and angiogenesis, but also have more sinister roles promoting conditions such as fibrogenesis.
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Potential Therapeutic Targets for Cardiac Fibrosis TGFβ, Angiotensin, Endothelin, CCN2, and PDGF, Partners in Fibroblast Activation
TL;DR: Recent observations concerning the contribution of TGF, endothelin-1, angiotensin II, Ang II, CCN2, and PDGF and to fibroblast activation in tissue repair and fibrosis and the potential utility of agents blocking these proteins in affecting the outcome of cardiac fibrosis are summarized.
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CTGF and SMADs, Maintenance of Scleroderma Phenotype Is Independent of SMAD Signaling
TL;DR: The maintenance of the fibrotic phenotype in scleroderma fibroblasts appears to be independent of SMAD-dependent TGFβ signaling, given CTGF's activities, which may contribute to the excessive scarring observed in this disorder.
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Regulation and function of connective tissue growth factor/CCN2 in tissue repair, scarring and fibrosis
TL;DR: A primary function of CTGF is to modulate and coordinate signaling responses involving cell surface proteoglycans, key components of the extracellular matrix, and growth factors, which regulates growth factor and receptor interactions, cell motility and mesenchymal cell activation and differentiation in tissue remodelling
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Gene regulation of connective tissue growth factor: new targets for antifibrotic therapy?
TL;DR: Outlining the mechanisms that underlie CTGF gene regulation in normal and fibrotic cells, might help design of future intervention strategies aiming at targeted specific interference with CTGF expression at sites of progressive fibrosis.