PMID- 23469847
OWN - NLM
STAT- MEDLINE
DCOM- 20140711
LR  - 20211021
IS  - 1996-3181 (Electronic)
IS  - 1871-5273 (Print)
IS  - 1871-5273 (Linking)
VI  - 12
IP  - 3
DP  - 2013 May 1
TI  - Biphasic mechanisms of neurovascular unit injury and protection in CNS diseases.
PG  - 302-15
AB  - In the past decade, evidence has emerged that there is a variety of bidirectional 
      cell-cell and/or cell-extracellular matrix interactions within the neurovascular 
      unit (NVU), which is composed of neuronal, glial, and vascular cells along with 
      extracellular matrix. Many central nervous system diseases, which lead to NVU 
      dysfunction, have common features such as glial activation/transformation and 
      vascular/blood-brain-barrier alteration. These phenomena show dual opposite 
      roles, harmful at acute phase and beneficial at chronic phase. This diverse 
      heterogeneity may induce biphasic clinical courses, i.e. degenerative and 
      regenerative processes in the context of dynamically coordinated cellcell/ 
      cell-matrix interactions in the NVU. A deeper understanding of the seemingly 
      contradictory actions in cellular levels is essential for NVU protection or 
      regeneration to suppress the deleterious inflammatory reactions and promote 
      adaptive remodeling after central nervous system injury. This mini-review will 
      present an overview of recent progress in the biphasic roles of the NVU and 
      discuss the clinical relevance of NVU responses associated with central nervous 
      system diseases, such as stroke and other chronic neurodegenerative diseases.
FAU - Maki, Takakuni
AU  - Maki T
AD  - Neuroprotection Research Laboratory, Massachusetts General Hospital East, 
      Charlestown, MA 02129, USA. karai@partners.org
FAU - Hayakawa, Kazuhide
AU  - Hayakawa K
FAU - Pham, Loc-Duyen D
AU  - Pham LD
FAU - Xing, Changhong
AU  - Xing C
FAU - Lo, Eng H
AU  - Lo EH
FAU - Arai, Ken
AU  - Arai K
LA  - eng
GR  - R01 NS065089/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United Arab Emirates
TA  - CNS Neurol Disord Drug Targets
JT  - CNS & neurological disorders drug targets
JID - 101269155
SB  - IM
MH  - Cell Communication/*physiology
MH  - Central Nervous System Diseases/*physiopathology
MH  - Endothelial Cells/*physiology
MH  - Humans
MH  - Nerve Regeneration/*physiology
MH  - Neuroglia/*physiology
MH  - Neurons/*physiology
PMC - PMC3845030
MID - NIHMS532529
EDAT- 2013/03/09 06:00
MHDA- 2014/07/12 06:00
PMCR- 2013/12/02
CRDT- 2013/03/09 06:00
PHST- 2012/09/01 00:00 [received]
PHST- 2012/10/11 00:00 [revised]
PHST- 2012/10/12 00:00 [accepted]
PHST- 2013/03/09 06:00 [entrez]
PHST- 2013/03/09 06:00 [pubmed]
PHST- 2014/07/12 06:00 [medline]
PHST- 2013/12/02 00:00 [pmc-release]
AID - CDTCNSND-EPUB-20130227-12 [pii]
AID - 10.2174/1871527311312030004 [doi]
PST - ppublish
SO  - CNS Neurol Disord Drug Targets. 2013 May 1;12(3):302-15. doi: 
      10.2174/1871527311312030004.