Transforming growth factor-β and its signaling pathway, Smads, is the major mechanism mediating fibrosis. However, the involvement of other signaling pathways and the interplay among these pathways in fibrosis remain largely unclear. In this chapter, we focus on the current understanding of the molecular basis of transforming growth factor-β signaling and its crosstalk pathways in renal fibrosis, which may be also applicable to a wide arrange of other disease conditions involving fibrosis. In addition, results from current studies also suggest that Smad signaling may be a final common pathway of fibrosis and targeting the Smad pathway may provide a new therapeutic strategy for tissue and/or organ fibrosis. © 2006 Humana Press Inc.
CITATION STYLE
Lan, H. Y., & Johnson, R. J. (2006). Glomerulonephritis and Smad signaling. In Principles of Molecular Medicine (pp. 629–635). Humana Press. https://doi.org/10.1007/978-1-59259-963-9_61
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