Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 21, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/ijms21114018
Keywords
chronic kidney disease; microenvironment; kidney fibrosis; macrophage-myofibroblast transition; inflammation
Funding
- Research Grants Council of Hong Kong [RGC 14106518, 14111019, 14121816, 14163317, 14117418, 14104019, C7018-16G]
- Innovation and Technology Fund of Hong Kong [ITS/068/18, PiH/009/19, PiH/010/19, PiH/394/19, InP/008/19, InP/009/19, InP/159/19]
- Chinese University of Hong Kong CUHK [4620528, 4054386, 4054440]
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Renal fibrosis is a common fate of chronic kidney diseases. Emerging studies suggest that unsolved inflammation will progressively transit into tissue fibrosis that finally results in an irreversible end-stage renal disease (ESRD). Renal inflammation recruits and activates immunocytes, which largely promotes tissue scarring of the diseased kidney. Importantly, studies have suggested a crucial role of innate immunity in the pathologic basis of kidney diseases. This review provides an update of both clinical and experimental information, focused on how innate immune signaling contributes to renal fibrogenesis. A better understanding of the underlying mechanisms may uncover a novel therapeutic strategy for ESRD.
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