PMID- 18272603
OWN - NLM
STAT- MEDLINE
DCOM- 20080613
LR  - 20220409
IS  - 1931-857X (Print)
IS  - 1522-1466 (Linking)
VI  - 294
IP  - 4
DP  - 2008 Apr
TI  - MCP-1/CCL2: a new diagnostic marker and therapeutic target for progressive renal 
      injury in diabetic nephropathy.
PG  - F697-701
LID - 10.1152/ajprenal.00016.2008 [doi]
AB  - Despite current therapies, many diabetic patients will suffer from declining 
      renal function in association with progressive kidney inflammation. Recently, 
      animal model studies have demonstrated that kidney macrophage accumulation is a 
      critical factor in the development of diabetic nephropathy. However, specific 
      anti-inflammatory strategies are not yet being considered for the treatment of 
      patients with diabetic renal injury. This review highlights the chemokine 
      monocyte chemoattractant protein-1 (MCP-1)/CC-chemokine ligand 2 as a major 
      promoter of inflammation, renal injury, and fibrosis in diabetic nephropathy. 
      Researchers have found that diabetes induces kidney MCP-1 production and that 
      urine MCP-1 levels can be used to assess renal inflammation in this disease. In 
      addition, genetic deletion and molecular blocking studies in rodents have 
      identified MCP-1 as an important therapeutic target for treating diabetic 
      nephropathy. Evidence also suggests that a polymorphism in the human MCP-1 gene 
      is associated with progressive kidney failure in type 2 diabetes, which may 
      identify patients at higher risk who need additional therapy. These findings 
      provide a strong rationale for developing specific therapies against MCP-1 and 
      inflammation in diabetic nephropathy.
FAU - Tesch, G H
AU  - Tesch GH
AD  - Dept. of Nephrology, Monash Medical Centre, 246 Clayton Rd., Clayton, Victoria 
      3168, Australia. greg.tesch@med.monash.edu.au
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20080213
PL  - United States
TA  - Am J Physiol Renal Physiol
JT  - American journal of physiology. Renal physiology
JID - 100901990
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/antagonists & inhibitors/deficiency/genetics/*physiology
MH  - Diabetes Mellitus, Type 2/genetics
MH  - Diabetic Nephropathies/genetics/*metabolism/therapy/urine
MH  - Disease Models, Animal
MH  - Humans
MH  - Macrophages/physiology
MH  - RNA, Messenger/genetics
RF  - 55
EDAT- 2008/02/15 09:00
MHDA- 2008/06/14 09:00
CRDT- 2008/02/15 09:00
PHST- 2008/02/15 09:00 [pubmed]
PHST- 2008/06/14 09:00 [medline]
PHST- 2008/02/15 09:00 [entrez]
AID - 00016.2008 [pii]
AID - 10.1152/ajprenal.00016.2008 [doi]
PST - ppublish
SO  - Am J Physiol Renal Physiol. 2008 Apr;294(4):F697-701. doi: 
      10.1152/ajprenal.00016.2008. Epub 2008 Feb 13.