Journal
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
Volume 8, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2020.00123
Keywords
TGF-beta; Smads; fibrosis; inflammation; mechanisms; therapy
Categories
Funding
- Research Grants Council of Hong Kong [GRF 14163317, 14117418, 14104019, R4012-18F, C7018-16G, T12-402/13N]
- Health and Medical Research Fund of Hong Kong [HMRF 05161326, TMP 09094, 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 Kong-Macao-Joint Labs Program from Guangdong Science and Technology [2019B121205005]
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Inflammation and fibrosis are two pathological features of chronic kidney disease (CKD). Transforming growth factor-beta (TGF-beta) has been long considered as a key mediator of renal fibrosis. In addition, TGF-beta also acts as a potent anti-inflammatory cytokine that negatively regulates renal inflammation. Thus, blockade of TGF-beta inhibits renal fibrosis while promoting inflammation, revealing a diverse role for TGF-beta in CKD. It is now well documented that TGF-beta 1 activates its downstream signaling molecules such as Smad3 and Smad3-dependent non-coding RNAs to transcriptionally and differentially regulate renal inflammation and fibrosis, which is negatively regulated by Smad7. Therefore, treatments by rebalancing Smad3/Smad7 signaling or by specifically targeting Smad3-dependent non-coding RNAs that regulate renal fibrosis or inflammation could be a better therapeutic approach. In this review, the paradoxical functions and underlying mechanisms by which TGF-beta 1 regulates in renal inflammation and fibrosis are discussed and novel therapeutic strategies for kidney disease by targeting downstream TGF-beta/Smad signaling and transcriptomes are highlighted.
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