PMID- 32060970
OWN - NLM
STAT- MEDLINE
DCOM- 20210826
LR  - 20240216
IS  - 1097-4547 (Electronic)
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 98
IP  - 7
DP  - 2020 Jul
TI  - Hypoxic-ischemic-related cerebrovascular changes and potential therapeutic 
      strategies in the neonatal brain.
PG  - 1468-1484
LID - 10.1002/jnr.24590 [doi]
AB  - Perinatal hypoxic-ischemic (HI)-related brain injury is an important cause of 
      morbidity and long-standing disability in newborns. The only currently approved 
      therapeutic strategy available to reduce brain injury in the newborn is 
      hypothermia. Therapeutic hypothermia can only be used to treat HI encephalopathy 
      in full-term infants and survivors remain at high risk for a wide spectrum of 
      neurodevelopmental abnormalities as a result of residual brain injury. Therefore, 
      there is an urgent need for adjunctive therapeutic strategies. Inflammation and 
      neurovascular damage are important factors that contribute to the pathophysiology 
      of HI-related brain injury and represent exciting potential targets for 
      therapeutic intervention. In this review, we address the role of each component 
      of the neurovascular unit (NVU) in the pathophysiology of HI-related injury in 
      the neonatal brain. Disruption of the blood-brain barrier (BBB) observed in the 
      early hours after an HI-related event is associated with a response at the basal 
      lamina level, which comprises astrocytes, pericytes, and immune cells, all of 
      which could affect BBB function to further exacerbate parenchymal injury. Future 
      research is required to determine potential drugs that could prevent or attenuate 
      neurovascular damage and/or augment repair. However, some studies have reported 
      beneficial effects of hypothermia, erythropoietin, stem cell therapy, 
      anti-cytokine therapy and metformin in ameliorating several different facets of 
      damage to the NVU after HI-related brain injury in the perinatal period.
CI  - (c) 2020 Wiley Periodicals, Inc.
FAU - Disdier, Clemence
AU  - Disdier C
AUID- ORCID: 0000-0003-3107-3459
AD  - Department of Pediatrics, Women & Infants Hospital of Rhode Island, The Alpert 
      Medical School of Brown University, Providence, RI, USA.
FAU - Stonestreet, Barbara S
AU  - Stonestreet BS
AUID- ORCID: 0000-0002-6532-7683
AD  - Department of Pediatrics, Women & Infants Hospital of Rhode Island, The Alpert 
      Medical School of Brown University, Providence, RI, USA.
LA  - eng
GR  - R21 NS096525/NS/NINDS NIH HHS/United States
GR  - R01 HD057100/HD/NICHD NIH HHS/United States
GR  - R44 NS084575/NS/NINDS NIH HHS/United States
GR  - P30 GM114750/GM/NIGMS NIH HHS/United States
GR  - R21 NS095130/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20200214
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Neuroprotective Agents)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Blood-Brain Barrier/drug effects/*physiopathology
MH  - Brain/drug effects/*physiopathology
MH  - Cerebrovascular Circulation/*drug effects
MH  - Disease Models, Animal
MH  - Humans
MH  - Hypothermia, Induced/*methods
MH  - Hypoxia-Ischemia, Brain/drug therapy/physiopathology/*therapy
MH  - Infant, Newborn
MH  - Neuroprotective Agents/pharmacology/*therapeutic use
PMC - PMC7242133
MID - NIHMS1554544
OTO - NOTNLM
OT  - brain injury
OT  - hypoxia ischemia
OT  - neonates
OT  - neurovascular unit
COIS- CONFLICT OF INTEREST There are no conflicts of interest to report.
EDAT- 2020/02/16 06:00
MHDA- 2021/08/27 06:00
PMCR- 2021/01/01
CRDT- 2020/02/16 06:00
PHST- 2019/09/24 00:00 [received]
PHST- 2020/01/20 00:00 [revised]
PHST- 2020/01/28 00:00 [accepted]
PHST- 2020/02/16 06:00 [pubmed]
PHST- 2021/08/27 06:00 [medline]
PHST- 2020/02/16 06:00 [entrez]
PHST- 2021/01/01 00:00 [pmc-release]
AID - 10.1002/jnr.24590 [doi]
PST - ppublish
SO  - J Neurosci Res. 2020 Jul;98(7):1468-1484. doi: 10.1002/jnr.24590. Epub 2020 Feb 
      14.