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Using the Bleomycin-Induced Model of Fibrosis to Study the Contribution of CCN Proteins to Scleroderma Fibrosis

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CCN Proteins

Part of the book series: Methods in Molecular Biology ((MIMB,volume 2582))

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Abstract

Approximately 45% of the deaths in the developed world result from conditions with a fibrotic component. Although no specific, focused anti-fibrotic therapies have been approved for clinical use, a long-standing concept is that targeting CCN proteins may be useful to treat fibrosis. Herein, we summarize current data supporting the concept that targeting CCN2 may be a viable anti-fibrotic approach to treat scleroderma. Testing this hypothesis has been made possible by using a mouse model of inflammation-driven skin and lung fibrosis.

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Acknowledgments

Work in Dr. Leask’s lab is supported by the Arthritis Society, the Canadian Institutes of Health Research, and the Natural Sciences and Engineering Research Council of Canada.

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Peidl, A., Nguyen, J., Chitturi, P., Riser, B.L., Leask, A. (2023). Using the Bleomycin-Induced Model of Fibrosis to Study the Contribution of CCN Proteins to Scleroderma Fibrosis. In: Takigawa, M. (eds) CCN Proteins. Methods in Molecular Biology, vol 2582. Humana, New York, NY. https://doi.org/10.1007/978-1-0716-2744-0_21

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  • DOI: https://doi.org/10.1007/978-1-0716-2744-0_21

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