Journal
FUTURE MEDICINAL CHEMISTRY
Volume 12, Issue 9, Pages 853-866Publisher
FUTURE SCI LTD
DOI: 10.4155/fmc-2020-0005
Keywords
immune cells; inflammation; renal fibrosis; TGF-beta; therapy
Categories
Funding
- Research Grants Council of Hong Kong [GRF 14121816, 14163317, 14117418, 14104019, R4012-18F, C7018-16G]
- Lui Che Woo Institute of Innovative Medicine (CARE)
- Health and Medical Research Fund of Hong Kong [HMRF 0314048, 05161326, 06173986, 14152321]
- Science and Technology Planning Project of Guangdong Province [2017B030314166]
- National Natural Science Foundation of China [81873261, 81903956]
- Project of Guangdong Province Administration of Traditional Chinese Medicine [20201133]
- Guangdong-Hong KongMacao-Joint Labs Program from Guangdong Science and Technology Department [2019B121205005]
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Renal fibrosis is a hallmark of chronic kidney disease. Although considerable achievements in the pathogenesis of renal fibrosis have been made, the underlying mechanisms of renal fibrosis remain largely to be explored. Now we have reached the consensus that TGF-beta is a master regulator of renal fibrosis. Indeed, TGF-beta regulates renal fibrosis via both canonical and noncanonical TGF-beta signaling. Moreover, ongoing renal inflammation promotes fibrosis as inflammatory cells such as macrophages, conventional T cells and mucosal-associated invariant T cells may directly or indirectly contribute to renal fibrosis, which is also tightly regulated by TGF-beta. However, anti-TGF-beta treatment for renal fibrosis remains ineffective and nonspecific. Thus, research into mechanisms and treatment of renal fibrosis remains highly challenging.
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