PMID- 23448509
OWN - NLM
STAT- MEDLINE
DCOM- 20131108
LR  - 20130422
IS  - 1440-1797 (Electronic)
IS  - 1320-5358 (Linking)
VI  - 18
IP  - 5
DP  - 2013 May
TI  - Role of interstitial inflammation in the pathogenesis of polycystic kidney 
      disease.
PG  - 317-30
LID - 10.1111/nep.12045 [doi]
AB  - 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)-alpha. Putative 
      upregulated inflammatory pathways include JAK-STAT and nuclear factor (NF)-kappaB 
      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.
CI  - (c) 2013 The Authors. Nephrology (c) 2013 Asian Pacific Society of Nephrology.
FAU - Ta, Michelle H T
AU  - Ta MH
AD  - Centre for Transplant and Renal Research, Westmead Millennium Institute, The 
      University of Sydney, Sydney, New South Wales, Australia. 
      michelle.ta@sydney.edu.au
FAU - Harris, David C H
AU  - Harris DC
FAU - Rangan, Gopala K
AU  - Rangan GK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Australia
TA  - Nephrology (Carlton)
JT  - Nephrology (Carlton, Vic.)
JID - 9615568
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - 0 (NF-kappa B)
RN  - 106441-73-0 (Osteopontin)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/therapeutic use
MH  - Cytokines/physiology
MH  - Genetic Predisposition to Disease
MH  - Humans
MH  - Inflammation/*complications
MH  - Inflammatory Bowel Diseases/*complications
MH  - Macrophages/physiology
MH  - Mutation
MH  - NF-kappa B/physiology
MH  - Osteopontin/physiology
MH  - Phagocytes/physiology
MH  - Polycystic Kidney Diseases/drug therapy/*etiology
EDAT- 2013/03/02 06:00
MHDA- 2013/11/10 06:00
CRDT- 2013/03/02 06:00
PHST- 2013/02/20 00:00 [accepted]
PHST- 2013/03/02 06:00 [entrez]
PHST- 2013/03/02 06:00 [pubmed]
PHST- 2013/11/10 06:00 [medline]
AID - 10.1111/nep.12045 [doi]
PST - ppublish
SO  - Nephrology (Carlton). 2013 May;18(5):317-30. doi: 10.1111/nep.12045.