PMID- 33540898
OWN - NLM
STAT- MEDLINE
DCOM- 20210409
LR  - 20210409
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 22
IP  - 3
DP  - 2021 Feb 2
TI  - Does C-C Motif Chemokine Ligand 2 (CCL2) Link Obesity to a Pro-Inflammatory 
      State?
LID - 10.3390/ijms22031500 [doi]
LID - 1500
AB  - The mechanisms of how obesity contributes to the development of cardio-metabolic 
      diseases are not entirely understood. Obesity is frequently associated with 
      adipose tissue dysfunction, characterized by, e.g., adipocyte hypertrophy, 
      ectopic fat accumulation, immune cell infiltration, and the altered secretion of 
      adipokines. Factors secreted from adipose tissue may induce and/or maintain a 
      local and systemic low-grade activation of the innate immune system. Attraction 
      of macrophages into adipose tissue and altered crosstalk between macrophages, 
      adipocytes, and other cells of adipose tissue are symptoms of metabolic 
      inflammation. Among several secreted factors attracting immune cells to adipose 
      tissue, chemotactic C-C motif chemokine ligand 2 (CCL2) (also described as 
      monocyte chemoattractant protein-1 (MCP-1)) has been shown to play a crucial role 
      in adipose tissue macrophage infiltration. In this review, we aimed to summarize 
      and discuss the current knowledge on CCL2 with a focus on its role in linking 
      obesity to cardio-metabolic diseases.
FAU - Dommel, Sebastian
AU  - Dommel S
AD  - Medical Department III-Endocrinology, Nephrology, Rheumatology, University of 
      Leipzig Medical Center, Germany Liebigstr. 20, 04103 Leipzig, Germany.
FAU - Bluher, Matthias
AU  - Bluher M
AUID- ORCID: 0000-0003-0208-2065
AD  - Medical Department III-Endocrinology, Nephrology, Rheumatology, University of 
      Leipzig Medical Center, Germany Liebigstr. 20, 04103 Leipzig, Germany.
AD  - Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG), 
      Helmholtz Zentrum Munchen, University of Leipzig and University Hospital Leipzig, 
      04103 Leipzig, Germany.
LA  - eng
GR  - 209933838/Deutsche Forschungsgemeinschaft/
PT  - Journal Article
PT  - Review
DEP - 20210202
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (CCL2 protein, human)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Neoplasm Proteins)
SB  - IM
MH  - Adipocytes/physiology
MH  - Adipose Tissue/metabolism
MH  - Animals
MH  - Autoimmune Diseases/genetics/metabolism
MH  - Cardiovascular Diseases/genetics/metabolism
MH  - Chemokine CCL2/deficiency/genetics/*physiology
MH  - Chemokines/metabolism
MH  - Humans
MH  - Inflammation/*complications/genetics/physiopathology
MH  - Insulin Resistance
MH  - Macrophages/physiology
MH  - Mesenchymal Stem Cells/metabolism
MH  - Metabolic Syndrome/genetics/metabolism
MH  - Mice
MH  - Mice, Knockout
MH  - Models, Animal
MH  - Molecular Targeted Therapy
MH  - Neoplasm Proteins/metabolism
MH  - Neoplasms/metabolism/pathology
MH  - Neural Tube Defects/genetics/metabolism
MH  - Obesity/*etiology/genetics/physiopathology
MH  - Polymorphism, Single Nucleotide
MH  - Signal Transduction
PMC - PMC7867366
OTO - NOTNLM
OT  - adipokine
OT  - adipose tissue
OT  - chemokine
OT  - inflammation
OT  - obesity
COIS- S.D. does not have any conflicts of interest to declare. M.B. received honoraria 
      as a consultant and speaker from Amgen, AstraZeneca, Bayer, Boehringer-Ingelheim, 
      Lilly, Novo Nordisk, Novartis, and Sanofi.
EDAT- 2021/02/06 06:00
MHDA- 2021/04/10 06:00
PMCR- 2021/02/02
CRDT- 2021/02/05 01:01
PHST- 2020/12/01 00:00 [received]
PHST- 2021/01/27 00:00 [revised]
PHST- 2021/01/29 00:00 [accepted]
PHST- 2021/02/05 01:01 [entrez]
PHST- 2021/02/06 06:00 [pubmed]
PHST- 2021/04/10 06:00 [medline]
PHST- 2021/02/02 00:00 [pmc-release]
AID - ijms22031500 [pii]
AID - ijms-22-01500 [pii]
AID - 10.3390/ijms22031500 [doi]
PST - epublish
SO  - Int J Mol Sci. 2021 Feb 2;22(3):1500. doi: 10.3390/ijms22031500.