Narrative review: fibrotic diseases: cellular and molecular mechanisms and novel therapies - PubMed (original) (raw)
Review
Narrative review: fibrotic diseases: cellular and molecular mechanisms and novel therapies
Joel Rosenbloom et al. Ann Intern Med. 2010.
Abstract
Abnormal and exaggerated deposition of extracellular matrix is the hallmark of many fibrotic diseases, including systemic sclerosis and pulmonary, liver, and kidney fibrosis. The spectrum of affected organs, the usually progressive nature of the fibrotic process, the large number of affected persons, and the absence of effective treatment pose an enormous challenge when treating fibrotic diseases. Delineation of the central role of transforming growth factor-beta (TGF-beta) and identification of the specific cellular receptors, kinases, and other mediators involved in the fibrotic process have provided a sound basis for development of effective therapies. The inhibition of signaling pathways activated by TGF-beta represents a novel therapeutic approach for the fibrotic disorders. One of these TGF-beta pathways results in the activation of the nonreceptor tyrosine kinase cellular Abelson (c-Abl), and c-Abl inhibitors, including imatinib mesylate, diminishing the fibrogenic effects of TGF-beta. Thus, recently acquired basic knowledge about the pathogenesis of the fibrotic process has enabled the development of novel therapeutic agents capable of modifying the deleterious effects of the fibrotic diseases.
Similar articles
- Human Fibrotic Diseases: Current Challenges in Fibrosis Research.
Rosenbloom J, Macarak E, Piera-Velazquez S, Jimenez SA. Rosenbloom J, et al. Methods Mol Biol. 2017;1627:1-23. doi: 10.1007/978-1-4939-7113-8_1. Methods Mol Biol. 2017. PMID: 28836191 Review. - TGF-beta signaling in vascular fibrosis.
Ruiz-Ortega M, Rodríguez-Vita J, Sanchez-Lopez E, Carvajal G, Egido J. Ruiz-Ortega M, et al. Cardiovasc Res. 2007 May 1;74(2):196-206. doi: 10.1016/j.cardiores.2007.02.008. Epub 2007 Feb 12. Cardiovasc Res. 2007. PMID: 17376414 Review. - The inhibitory effect of ginsan on TGF-β mediated fibrotic process.
Ahn JY, Kim MH, Lim MJ, Park S, Lee SL, Yun YS, Song JY. Ahn JY, et al. J Cell Physiol. 2011 May;226(5):1241-7. doi: 10.1002/jcp.22452. J Cell Physiol. 2011. PMID: 20945375 - Inhibition of PDGF, VEGF and FGF signalling attenuates fibrosis.
Chaudhary NI, Roth GJ, Hilberg F, Müller-Quernheim J, Prasse A, Zissel G, Schnapp A, Park JE. Chaudhary NI, et al. Eur Respir J. 2007 May;29(5):976-85. doi: 10.1183/09031936.00152106. Epub 2007 Feb 14. Eur Respir J. 2007. PMID: 17301095 - Imatinib mesylate reduces production of extracellular matrix and prevents development of experimental dermal fibrosis.
Distler JH, Jüngel A, Huber LC, Schulze-Horsel U, Zwerina J, Gay RE, Michel BA, Hauser T, Schett G, Gay S, Distler O. Distler JH, et al. Arthritis Rheum. 2007 Jan;56(1):311-22. doi: 10.1002/art.22314. Arthritis Rheum. 2007. PMID: 17195235
Cited by
- Pivotal role for decorin in angiogenesis.
Järveläinen H, Sainio A, Wight TN. Järveläinen H, et al. Matrix Biol. 2015 Apr;43:15-26. doi: 10.1016/j.matbio.2015.01.023. Epub 2015 Feb 7. Matrix Biol. 2015. PMID: 25661523 Free PMC article. Review. - Profibrotic up-regulation of glucose transporter 1 by TGF-β involves activation of MEK and mammalian target of rapamycin complex 2 pathways.
Andrianifahanana M, Hernandez DM, Yin X, Kang JH, Jung MY, Wang Y, Yi ES, Roden AC, Limper AH, Leof EB. Andrianifahanana M, et al. FASEB J. 2016 Nov;30(11):3733-3744. doi: 10.1096/fj.201600428R. Epub 2016 Aug 1. FASEB J. 2016. PMID: 27480571 Free PMC article. - FibronectinEDA promotes chronic cutaneous fibrosis through Toll-like receptor signaling.
Bhattacharyya S, Tamaki Z, Wang W, Hinchcliff M, Hoover P, Getsios S, White ES, Varga J. Bhattacharyya S, et al. Sci Transl Med. 2014 Apr 16;6(232):232ra50. doi: 10.1126/scitranslmed.3008264. Sci Transl Med. 2014. PMID: 24739758 Free PMC article. - Decorin is a pivotal effector in the extracellular matrix and tumour microenvironment.
Zhang W, Ge Y, Cheng Q, Zhang Q, Fang L, Zheng J. Zhang W, et al. Oncotarget. 2018 Jan 3;9(4):5480-5491. doi: 10.18632/oncotarget.23869. eCollection 2018 Jan 12. Oncotarget. 2018. PMID: 29435195 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Miscellaneous