PMID- 24523386
OWN - NLM
STAT- MEDLINE
DCOM- 20140615
LR  - 20220331
IS  - 1522-1466 (Electronic)
IS  - 1931-857X (Print)
IS  - 1522-1466 (Linking)
VI  - 306
IP  - 8
DP  - 2014 Apr 15
TI  - Role of Toll-like receptor-4 in renal graft ischemia-reperfusion injury.
PG  - F801-11
LID - 10.1152/ajprenal.00469.2013 [doi]
AB  - Toll-like receptor-4 (TLR-4) has been increasingly recognized as playing a 
      critical role in the pathogenesis of ischemia-reperfusion injury (IRI) of renal 
      grafts. This review provides a detailed overview of the new understanding of the 
      involvement of TLR-4 in ischemia-reperfusion injury of renal grafts and its 
      clinical significance in renal transplantation. TLR-4 not only responds to 
      exogenous microbial motifs but can also recognize molecules which are released by 
      stressed and necrotic cells, as well as degraded products of endogenous 
      macromolecules. Upregulation of TLR-4 is found in tubular epithelial cells, 
      vascular endothelial cells, and infiltrating leukocytes during renal 
      ischemia-reperfusion injury, which is induced by massive release of endogenous 
      damage-associated molecular pattern molecules such as high-mobility group box 
      chromosomal protein 1. Activation of TLR-4 promotes the release of 
      proinflammatory mediators, facilitates leukocyte migration and infiltration, 
      activates the innate and adaptive immune system, and potentiates renal fibrosis. 
      TLR-4 inhibition serves as the target of pharmacological agents, which could 
      attenuate ischemia-reperfusion injury and associated delayed graft function and 
      allograft rejection. There is evidence in the literature showing that targeting 
      TLR-4 could improve long-term transplantation outcomes. Given the pivotal role of 
      TLR-4 in ischemia-reperfusion injury and associated delayed graft function and 
      allograft rejection, inhibition of TLR-4 using pharmacological agents could be 
      beneficial for long-term graft survival.
FAU - Zhao, Hailin
AU  - Zhao H
AD  - Anaesthetics, Pain Medicine, and Intensive Care, Dept. of Surgery and Cancer, 
      Faculty of Medicine, Imperial College London, Chelsea and Westminster Hospital, 
      London, UK. d.ma@imperial.ac.uk.
FAU - Perez, Jessica Santivanez
AU  - Perez JS
FAU - Lu, Kaizhi
AU  - Lu K
FAU - George, Andrew J T
AU  - George AJ
FAU - Ma, Daqing
AU  - Ma D
LA  - eng
GR  - Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20140212
PL  - United States
TA  - Am J Physiol Renal Physiol
JT  - American journal of physiology. Renal physiology
JID - 100901990
RN  - 0 (Biglycan)
RN  - 0 (HMGB1 Protein)
RN  - 0 (Heat-Shock Proteins)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (TLR4 protein, human)
RN  - 0 (Toll-Like Receptor 4)
SB  - IM
MH  - Animals
MH  - Biglycan/physiology
MH  - Graft Rejection
MH  - HMGB1 Protein/physiology
MH  - Heat-Shock Proteins/physiology
MH  - Humans
MH  - Immunity, Innate/physiology
MH  - Kidney Transplantation/*adverse effects
MH  - Kidney Tubular Necrosis, Acute/etiology
MH  - Myeloid Differentiation Factor 88/physiology
MH  - Polymorphism, Genetic
MH  - Reperfusion Injury/*physiopathology
MH  - Signal Transduction
MH  - Toll-Like Receptor 4/genetics/*physiology
PMC - PMC3989634
OTO - NOTNLM
OT  - Toll-like receptor 4
OT  - delayed graft function
OT  - ischemia-reperfusion injury
OT  - renal graft failure
OT  - renal transplantation
EDAT- 2014/02/14 06:00
MHDA- 2014/06/16 06:00
PMCR- 2015/04/15
CRDT- 2014/02/14 06:00
PHST- 2014/02/14 06:00 [entrez]
PHST- 2014/02/14 06:00 [pubmed]
PHST- 2014/06/16 06:00 [medline]
PHST- 2015/04/15 00:00 [pmc-release]
AID - ajprenal.00469.2013 [pii]
AID - F-00469-2013 [pii]
AID - 10.1152/ajprenal.00469.2013 [doi]
PST - ppublish
SO  - Am J Physiol Renal Physiol. 2014 Apr 15;306(8):F801-11. doi: 
      10.1152/ajprenal.00469.2013. Epub 2014 Feb 12.