PMID- 28566450
OWN - NLM
STAT- MEDLINE
DCOM- 20170828
LR  - 20220330
IS  - 1470-8736 (Electronic)
IS  - 0143-5221 (Linking)
VI  - 131
IP  - 12
DP  - 2017 Jun 1
TI  - Monocyte subtypes and the CCR2 chemokine receptor in cardiovascular disease.
PG  - 1215-1224
LID - 10.1042/CS20170009 [doi]
AB  - Monocytes circulate in the blood and migrate to inflammatory tissues, but their 
      functions can be either detrimental or beneficial, depending on their phenotypes. 
      In humans, classical monocytes are inflammatory cluster of differentiation 
      (CD)14(++)CD16(-)CCR2(++) cells originated from the bone marrow or spleen 
      reservoirs and comprise >/=92% of monocytes. Intermediate monocytes 
      (CD14(++)CD16(+)CCR2(+)) are involved in the production of anti-inflammatory 
      cytokines [such as interleukin (IL)-10], reactive oxygen species (ROS), and 
      proinflammatory mediators [such as tumor necrosis factor-alpha (TNF-alpha) and IL-1beta). 
      Nonclassical monocytes (CD14(+)CD16(++)CCR2(-)) are patrolling cells involved in 
      tissue repair and debris removal from the vasculature. Many studies in both 
      humans and animals have shown the importance of monocyte chemoattractant 
      protein-1 (MCP-1) and its receptor [chemokine receptor of MCP-1 (CCR2)] in 
      pathologies, such as atherosclerosis and myocardial infarction (MI). This review 
      presents the importance of these monocyte subsets in cardiovascular diseases 
      (CVDs), and sheds light on new strategies for the blocking of the MCP-1/CCR2 axis 
      as a therapeutic goal for treating vascular disorders.
CI  - (c) 2017 The Author(s). published by Portland Press Limited on behalf of the 
      Biochemical Society.
FAU - Franca, Carolina N
AU  - Franca CN
AD  - Santo Amaro University-Health Sciences Post Graduation, Sao Paulo - SP, Brazil 
      carolufscar24@gmail.com.
AD  - Federal University of Sao Paulo, Department of Medicine, Cardiology Division, Sao 
      Paulo - SP, Brazil.
FAU - Izar, Maria C O
AU  - Izar MCO
AD  - Federal University of Sao Paulo, Department of Medicine, Cardiology Division, Sao 
      Paulo - SP, Brazil.
FAU - Hortencio, Marinella N S
AU  - Hortencio MNS
AD  - Santo Amaro University-Health Sciences Post Graduation, Sao Paulo - SP, Brazil.
FAU - do Amaral, Jonatas B
AU  - do Amaral JB
AD  - Federal University of Sao Paulo, Department of Otorhinolaryngology, Head and Neck 
      Surgery, Sao Paulo - SP, Brazil.
FAU - Ferreira, Carlos E S
AU  - Ferreira CES
AD  - Albert Einstein Israeli Hospital, Sao Paulo - SP, Brazil.
FAU - Tuleta, Izabela D
AU  - Tuleta ID
AD  - Medizinische Klinik und Poliklinik II-Universitatsklinikum Bonn, Bonn - North 
      Rhine-Westphalia, Germany.
FAU - Fonseca, Francisco A H
AU  - Fonseca FAH
AD  - Federal University of Sao Paulo, Department of Medicine, Cardiology Division, Sao 
      Paulo - SP, Brazil.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Clin Sci (Lond)
JT  - Clinical science (London, England : 1979)
JID - 7905731
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (CCL2 protein, human)
RN  - 0 (CCR2 protein, human)
RN  - 0 (Cardiovascular Agents)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Ligands)
RN  - 0 (Receptors, CCR2)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/therapeutic use
MH  - Cardiovascular Agents/therapeutic use
MH  - Cardiovascular Diseases/drug therapy/immunology/*metabolism
MH  - Chemokine CCL2/antagonists & inhibitors/*metabolism
MH  - Humans
MH  - Ligands
MH  - Monocytes/classification/drug effects/immunology/*metabolism
MH  - Phenotype
MH  - Receptors, CCR2/antagonists & inhibitors/*metabolism
MH  - Signal Transduction
OTO - NOTNLM
OT  - atherosclerosis
OT  - chemokine receptor CCR2
OT  - monocyte chemoattractant protein-1
OT  - monocyte subtypes
OT  - myocardial infarction
EDAT- 2017/06/02 06:00
MHDA- 2017/08/29 06:00
CRDT- 2017/06/02 06:00
PHST- 2017/01/06 00:00 [received]
PHST- 2017/02/17 00:00 [revised]
PHST- 2017/02/24 00:00 [accepted]
PHST- 2017/06/02 06:00 [entrez]
PHST- 2017/06/02 06:00 [pubmed]
PHST- 2017/08/29 06:00 [medline]
AID - CS20170009 [pii]
AID - 10.1042/CS20170009 [doi]
PST - ppublish
SO  - Clin Sci (Lond). 2017 Jun 1;131(12):1215-1224. doi: 10.1042/CS20170009.