Topics

No keywords indexed for this article. Browse by subject →

References
251
[1]
Eddy, A. A. & Neilson, E. G. Chronic kidney disease progression. J. Am. Soc. Nephrol. 17, 2964–2966 (2006). 10.1681/asn.2006070704
[2]
Bottinger, E. P. & Bitzer, M. TGF-β signaling in renal disease. J. Am. Soc. Nephrol. 13, 2600–2610 (2002). 10.1097/01.asn.0000033611.79556.ae
[3]
Eddy, A. A. Overview of the cellular and molecular basis of kidney fibrosis. Kidney Int. Suppl. (2011) 4, 2–8 (2014). 10.1038/kisup.2014.2
[4]
Sharma, K. et al. Increased renal production of transforming growth factor-β1 in patients with type II diabetes. Diabetes 46, 854–859 (1997). 10.2337/diab.46.5.854
[5]
Yamamoto, T., Nakamura, T., Noble, N. A., Ruoslahti, E. & Border, W. A. Expression of transforming growth factor β is elevated in human and experimental diabetic nephropathy. Proc. Natl Acad. Sci. USA 90, 1814–1818 (1993). 10.1073/pnas.90.5.1814
[6]
Yoshioka, K. et al. Transforming growth factor-beta protein and mRNA in glomeruli in normal and diseased human kidneys. Lab. Invest. 68, 154–163 (1993).
[7]
Border, W. A., Okuda, S., Languino, L. R., Sporn, M. B. & Ruoslahti, E. Suppression of experimental glomerulonephritis by antiserum against transforming growth factor β1. Nature 346, 371–374 (1990). 10.1038/346371a0
[8]
Isaka, Y. et al. Glomerulosclerosis induced by in vivo transfection of transforming growth factor-beta or platelet-derived growth factor gene into the rat kidney. J. Clin. Invest. 92, 2597–2601 (1993). 10.1172/jci116874
[9]
Moon, J. A., Kim, H. T., Cho, I. S., Sheen, Y. Y. & Kim, D. K. IN-1130, a novel transforming growth factor-β type I receptor kinase (ALK5) inhibitor, suppresses renal fibrosis in obstructive nephropathy. Kidney Int. 70, 1234–1243 (2006). 10.1038/sj.ki.5001775
[10]
Russo, L. M., del Re, E., Brown, D. & Lin, H. Y. Evidence for a role of transforming growth factor (TGF)-β1 in the induction of postglomerular albuminuria in diabetic nephropathy: amelioration by soluble TGF-β type II receptor. Diabetes 56, 380–388 (2007). 10.2337/db06-1018
[11]
Sato, M., Muragaki, Y., Saika, S., Roberts, A. B. & Ooshima, A. Targeted disruption of TGF-β1/Smad3 signaling protects against renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction. J. Clin. Invest. 112, 1486–1494 (2003). 10.1172/jci200319270
[12]
Meng, X. M., Chung, A. C. & Lan, H. Y. Role of the TGF-β/BMP-7/Smad pathways in renal diseases. Clin. Sci. (Lond.) 124, 243–254 (2013). 10.1042/cs20120252
[13]
Zhang, Y. E. Non-Smad pathways in TGF-β signaling. Cell Res. 19, 128–139 (2009). 10.1038/cr.2008.328
[14]
Yu, L., Border, W. A., Huang, Y. & Noble, N. A. TGF-β isoforms in renal fibrogenesis. Kidney Int. 64, 844–856 (2003). 10.1046/j.1523-1755.2003.00162.x
[15]
Xu, P., Liu, J. & Derynck, R. Post-translational regulation of TGF-β receptor and Smad signaling. FEBS Lett. 586, 1871–1884 (2012). 10.1016/j.febslet.2012.05.010
[16]
Sanderson, N. et al. Hepatic expression of mature transforming growth factor β 1 in transgenic mice results in multiple tissue lesions. Proc. Natl Acad. Sci. USA 92, 2572–2576 (1995). 10.1073/pnas.92.7.2572
[17]
Robertson, I. B. et al. Latent TGF-β-binding proteins. Matrix Biol. 47, 44–53 (2015). 10.1016/j.matbio.2015.05.005
[18]
Annes, J. P., Munger, J. S. & Rifkin, D. B. Making sense of latent TGFβ activation. J. Cell Sci. 116, 217–224 (2003). 10.1242/jcs.00229
[19]
Probst-Kepper, M., Balling, R. & Buer, J. FOXP3: required but not sufficient. The role of GARP (LRRC32) as a safeguard of the regulatory phenotype. Curr. Mol. Med. 10, 533–539 (2010).
[20]
Mice overexpressing latent TGF-β1 are protected against renal fibrosis in obstructive kidney disease

Xiao R. Huang, Arthur C. K. Chung, Xiao J. Wang et al.

American Journal of Physiology-Renal Physiology 2008 10.1152/ajprenal.00021.2008
[21]
Huang, X. R., Chung, A. C., Zhou, L., Wang, X. J. & Lan, H. Y. Latent TGF-β1 protects against crescentic glomerulonephritis. J. Am. Soc. Nephrol. 19, 233–242 (2008). 10.1681/asn.2007040484
[22]
Border, W. A., Okuda, S., Languino, L. R. & Ruoslahti, E. Transforming growth factor-β regulates production of proteoglycans by mesangial cells. Kidney Int. 37, 689–695 (1990). 10.1038/ki.1990.35
[23]
Haberstroh, U. et al. TGF-β stimulates rat mesangial cell proliferation in culture: role of PDGF beta-receptor expression. Am. J. Physiol. 264, F199–F205 (1993).
[24]
Wilson, H. M. et al. Effect of transforming growth factor-beta 1 on plasminogen activators and plasminogen activator inhibitor-1 in renal glomerular cells. Exp. Nephrol. 1, 343–350 (1993).
[25]
Lopez-Hernandez, F. J. & Lopez-Novoa, J. M. Role of TGF-β in chronic kidney disease: an integration of tubular, glomerular and vascular effects. Cell Tissue Res. 347, 141–154 (2012). 10.1007/s00441-011-1275-6
[26]
Gruden, G., Perin, P. C. & Camussi, G. Insight on the pathogenesis of diabetic nephropathy from the study of podocyte and mesangial cell biology. Curr. Diabetes Rev. 1, 27–40 (2005). 10.2174/1573399052952622
[27]
Neelisetty, S. et al. Renal fibrosis is not reduced by blocking transforming growth factor-β signaling in matrix-producing interstitial cells. Kidney Int. 88, 503–514 (2015). 10.1038/ki.2015.51
[28]
Meng, X. M. et al. Diverse roles of TGF-β receptor II in renal fibrosis and inflammation in vivo and in vitro. J. Pathol. 227, 175–188 (2012). 10.1002/path.3976
[29]
Gewin, L. et al. TGF-β receptor deletion in the renal collecting system exacerbates fibrosis. J. Am. Soc. Nephrol. 21, 1334–1343 (2010). 10.1681/asn.2010020147
[30]
Lebrin, F., Deckers, M., Bertolino, P. & Ten Dijke, P. TGF-β receptor function in the endothelium. Cardiovasc. Res. 65, 599–608 (2005). 10.1016/j.cardiores.2004.10.036
[31]
Das, R. et al. Upregulation of mitochondrial Nox4 mediates TGF-β-induced apoptosis in cultured mouse podocytes. Am. J. Physiol. Renal Physiol. 306, F155–F167 (2014). 10.1152/ajprenal.00438.2013
[32]
Mack, M. & Yanagita, M. Origin of myofibroblasts and cellular events triggering fibrosis. Kidney Int. 87, 297–307 (2015). 10.1038/ki.2014.287
[33]
Chen, S. J. et al. Stimulation of type I collagen transcription in human skin fibroblasts by TGF-β: involvement of Smad 3. J. Invest. Dermatol. 112, 49–57 (1999). 10.1046/j.1523-1747.1999.00477.x
[34]
Yuan, W. & Varga, J. Transforming growth factor-β repression of matrix metalloproteinase-1 in dermal fibroblasts involves Smad3. J. Biol. Chem. 276, 38502–38510 (2001). 10.1074/jbc.m107081200
[35]
Dennler, S. et al. Direct binding of Smad3 and Smad4 to critical TGF β-inducible elements in the promoter of human plasminogen activator inhibitor-type 1 gene. EMBO J. 17, 3091–3100 (1998). 10.1093/emboj/17.11.3091
[36]
Piek, E. et al. Functional characterization of transforming growth factor β signaling in Smad2- and Smad3-deficient fibroblasts. J. Biol. Chem. 276, 19945–19953 (2001). 10.1074/jbc.m102382200
[37]
Goumans, M. J. & Mummery, C. Functional analysis of the TGFbeta receptor/Smad pathway through gene ablation in mice. Int. J. Dev. Biol. 44, 253–265 (2000).
[38]
Inazaki, K. et al. Smad3 deficiency attenuates renal fibrosis, inflammation, and apoptosis after unilateral ureteral obstruction. Kidney Int. 66, 597–604 (2004). 10.1111/j.1523-1755.2004.00779.x
[39]
Kim, J. H., Kim, B. K., Moon, K. C., Hong, H. K. & Lee, H. S. Activation of the TGF-β/Smad signaling pathway in focal segmental glomerulosclerosis. Kidney Int. 64, 1715–1721 (2003). 10.1046/j.1523-1755.2003.00288.x
[40]
Fujimoto, M. et al. Mice lacking Smad3 are protected against streptozotocin-induced diabetic glomerulopathy. Biochem. Biophys. Res. Commun. 305, 1002–1007 (2003). 10.1016/s0006-291x(03)00885-4
[41]
Zhou, L. et al. Mechanism of chronic aristolochic acid nephropathy: role of Smad3. Am. J. Physiol. Renal Physiol. 298, F1006–F1017 (2010). 10.1152/ajprenal.00675.2009
[42]
Meng, X. M. et al. Smad2 protects against TGF-β/Smad3-mediated renal fibrosis. J. Am. Soc. Nephrol. 21, 1477–1487 (2010). 10.1681/asn.2009121244
[43]
Tsuchida, K., Zhu, Y., Siva, S., Dunn, S. R. & Sharma, K. Role of Smad4 on TGF-β-induced extracellular matrix stimulation in mesangial cells. Kidney Int. 63, 2000–2009 (2003). 10.1046/j.1523-1755.2003.00009.x
[44]
Meng, X. M. et al. Disruption of Smad4 impairs TGF-β/Smad3 and Smad7 transcriptional regulation during renal inflammation and fibrosis in vivo and in vitro. Kidney Int. 81, 266–279 (2012). 10.1038/ki.2011.327
[45]
Yan, X. & Chen, Y. G. Smad7: not only a regulator, but also a cross-talk mediator of TGF-β signalling. Biochem. J. 434, 1–10 (2011). 10.1042/bj20101827
[46]
Shi, Y. & Massague, J. Mechanisms of TGF-β signaling from cell membrane to the nucleus. Cell 113, 685–700 (2003). 10.1016/s0092-8674(03)00432-x
[47]
Down-regulation of Smad7 expression by ubiquitin-dependent degradation contributes to renal fibrosis in obstructive nephropathy in mice

Hirotaka Fukasawa, Tatsuo Yamamoto, Akashi Togawa et al.

Proceedings of the National Academy of Sciences 2004 10.1073/pnas.0400035101
[48]
Chung, A. C. et al. Disruption of the Smad7 gene promotes renal fibrosis and inflammation in unilateral ureteral obstruction (UUO) in mice. Nephrol. Dial. Transplant. 24, 1443–1454 (2009). 10.1093/ndt/gfn699
[49]
Chen, H. Y. et al. The protective role of Smad7 in diabetic kidney disease: mechanism and therapeutic potential. Diabetes 60, 590–601 (2011). 10.2337/db10-0403
[50]
Liu, G. X. et al. Disruption of Smad7 promotes ANG II-mediated renal inflammation and fibrosis via Sp1-TGF-β/Smad3-NF.κB-dependent mechanisms in mice. PLoS ONE 8, e53573 (2013). 10.1371/journal.pone.0053573

Showing 50 of 251 references

Cited By
3,104
Journal of Controlled Release
Nature
Science Translational Medicine
Frontiers in Pharmacology
The American Journal of Chinese Med...
Oxidative Medicine and Cellular Lon...
Metrics
3,104
Citations
251
References
Details
Published
Apr 25, 2016
Vol/Issue
12(6)
Pages
325-338
License
View
Cite This Article
Xiao-Ming Meng, David J. Nikolic-Paterson, Hui Yao Lan (2016). TGF-β: the master regulator of fibrosis. Nature Reviews Nephrology, 12(6), 325-338. https://doi.org/10.1038/nrneph.2016.48
Related

You May Also Like