Journal
NEPHROLOGY
Volume 18, Issue 5, Pages 317-330Publisher
WILEY
DOI: 10.1111/nep.12045
Keywords
inflammation; macrophage; nuclear factor-B; polycystic kidney disease; tumour necrosis factor-
Categories
Funding
- Michael Stern Polycystic Kidney Disease Research Fellowship
- University of Sydney
- NHMRC [632647, 457575]
Ask authors/readers for more resources
Interstitial infiltrates, consisting of macrophages and other inflammatory cells, have been consistently reported in human and animal models of polycystic kidney diseases (PKD). However, the mechanisms underlying this inflammation are not well defined. Evidence suggests that interstitial inflammation in PKD is driven by pro-inflammatory chemoattractants such as monocyte chemoattractant protein-1 (MCP-1), and cytokines such as tumour necrosis factor (TNF)-. Putative upregulated inflammatory pathways include JAK-STAT and nuclear factor (NF)-B signalling. In addition, the genetic mutations of PKD may further complicate the relationship between inflammation and cystic disease, by increasing the susceptibility to inflammatory injury, and facilitating interactions between the genetically determined cystoproteins and biological mediators of inflammation. Moreover, the roles of interstitial inflammation in promoting cyst growth and progression to kidney failure in PKD are not clearly understood. Although anti-inflammatory therapies have attenuated cystogenesis in animal models, inflammatory cells may also have reparative actions. Thus, in developing therapies for PKD, it is prudent to consider the potential negative outcomes of ablating inflammation, and whether it is more viable to target certain inflammatory pathways over others.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available