Journal
SEMINARS IN NEPHROLOGY
Volume 27, Issue 3, Pages 309-320Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.semnephrol.2007.02.009
Keywords
fibrosis; chronic kidney disease; cell biology; signal transduction; apoptosis
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Funding
- NIDDK NIH HHS [U01DK060995, R01DK56077, P50DK064236-01003, R01DK60043] Funding Source: Medline
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Chronic progressive kidney diseases typically are characterized by loss of differentiated epithelial cells and activation of mesenchymal cell populations leading to renal fibrosis in response to a broad range of diverse renal injuries. Recent evidence has indicated that epithelial microinjury leads to unbalanced epithelial-mesenchymal communication to initiate the fibrotic response. Transforming growth factors beta constitute a large family of cytokines that control key cellular responses in development and tissue repair. Activation of autocrine and paracrine transforming growth factor-beta signaling cascades in the context of epithelial microinjuries initiate a variety of cell type- dependent signaling and activity profiles, including epithelial apoptosis and epithelial-to-mesenchymal transition, that trigger fibrogenic foci and initiate progressive fibrogenesis in chronic renal injury.
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