PMID- 37909340
OWN - NLM
STAT- MEDLINE
DCOM- 20240115
LR  - 20240322
IS  - 1098-1136 (Electronic)
IS  - 0894-1491 (Print)
IS  - 0894-1491 (Linking)
VI  - 72
IP  - 3
DP  - 2024 Mar
TI  - Key roles of glial cells in the encephalopathy of prematurity.
PG  - 475-503
LID - 10.1002/glia.24474 [doi]
AB  - Across the globe, approximately one in 10 babies are born preterm, that is, 
      before 37 weeks of a typical 40 weeks of gestation. Up to 50% of preterm born 
      infants develop brain injury, encephalopathy of prematurity (EoP), that 
      substantially increases their risk for developing lifelong defects in motor 
      skills and domains of learning, memory, emotional regulation, and cognition. We 
      are still severely limited in our abilities to prevent or predict preterm birth. 
      No longer just the "support cells," we now clearly understand that during 
      development glia are key for building a healthy brain. Glial dysfunction is a 
      hallmark of EoP, notably, microgliosis, astrogliosis, and oligodendrocyte injury. 
      Our knowledge of glial biology during development is exponentially expanding but 
      hasn't developed sufficiently for development of effective neuroregenerative 
      therapies. This review summarizes the current state of knowledge for the roles of 
      glia in infants with EoP and its animal models, and a description of known 
      glial-cell interactions in the context of EoP, such as the roles for 
      border-associated macrophages. The field of perinatal medicine is relatively 
      small but has worked passionately to improve our understanding of the etiology of 
      EoP coupled with detailed mechanistic studies of pre-clinical and human cohorts. 
      A primary finding from this review is that expanding our collaborations with 
      computational biologists, working together to understand the complexity of glial 
      subtypes, glial maturation, and the impacts of EoP in the short and long term 
      will be key to the design of therapies that improve outcomes.
CI  - (c) 2023 The Authors. GLIA published by Wiley Periodicals LLC.
FAU - Van Steenwinckel, Juliette
AU  - Van Steenwinckel J
AUID- ORCID: 0000-0003-3463-4856
AD  - NeuroDiderot, INSERM, Universite Paris Cite, Paris, France.
FAU - Bokobza, Cindy
AU  - Bokobza C
AD  - NeuroDiderot, INSERM, Universite Paris Cite, Paris, France.
FAU - Laforge, Mireille
AU  - Laforge M
AUID- ORCID: 0000-0002-1892-5250
AD  - NeuroDiderot, INSERM, Universite Paris Cite, Paris, France.
FAU - Shearer, Isabelle K
AU  - Shearer IK
AD  - School of Health and Biomedical Sciences, STEM College, RMIT University, 
      Bundoora, Victoria, Australia.
FAU - Miron, Veronique E
AU  - Miron VE
AD  - Barlo Multiple Sclerosis Centre, St. Michael's Hospital, Toronto, Ontario, 
      Canada.
AD  - Department of Immunology, University of Toronto, Toronto, Ontario, Canada.
AD  - College of Medicine and Veterinary Medicine, The Dementia Research Institute at 
      The University of Edinburgh, Edinburgh, UK.
FAU - Rua, Rejane
AU  - Rua R
AD  - CNRS, INSERM, Centre d'Immunologie de Marseille-Luminy (CIML), Turing Centre for 
      Living Systems, Aix-Marseille University, Marseille, France.
FAU - Matta, Samantha M
AU  - Matta SM
AD  - School of Health and Biomedical Sciences, STEM College, RMIT University, 
      Bundoora, Victoria, Australia.
FAU - Hill-Yardin, Elisa L
AU  - Hill-Yardin EL
AD  - School of Health and Biomedical Sciences, STEM College, RMIT University, 
      Bundoora, Victoria, Australia.
FAU - Fleiss, Bobbi
AU  - Fleiss B
AD  - NeuroDiderot, INSERM, Universite Paris Cite, Paris, France.
AD  - School of Health and Biomedical Sciences, STEM College, RMIT University, 
      Bundoora, Victoria, Australia.
FAU - Gressens, Pierre
AU  - Gressens P
AUID- ORCID: 0000-0002-0909-4221
AD  - NeuroDiderot, INSERM, Universite Paris Cite, Paris, France.
LA  - eng
GR  - MR/V031260/1/MRC_/Medical Research Council/United Kingdom
GR  - ERC_/European Research Council/International
PT  - Journal Article
PT  - Review
DEP - 20231101
PL  - United States
TA  - Glia
JT  - Glia
JID - 8806785
SB  - IM
MH  - Infant
MH  - Pregnancy
MH  - Animals
MH  - Female
MH  - Infant, Newborn
MH  - Humans
MH  - *Premature Birth
MH  - Infant, Premature
MH  - Neuroglia
MH  - Brain
MH  - *Brain Injuries
PMC - PMC10952406
OTO - NOTNLM
OT  - astrocytes
OT  - cytokine and chemokine receptors
OT  - development
OT  - growth factor
OT  - mechanisms of glia cell injury
OT  - microglial cells
OT  - oligodendrocytes
COIS- The authors declare no conflicts of interest.
EDAT- 2023/11/01 12:44
MHDA- 2024/01/15 12:43
PMCR- 2024/03/20
CRDT- 2023/11/01 06:55
PHST- 2023/09/17 00:00 [revised]
PHST- 2023/07/19 00:00 [received]
PHST- 2023/09/19 00:00 [accepted]
PHST- 2024/01/15 12:43 [medline]
PHST- 2023/11/01 12:44 [pubmed]
PHST- 2023/11/01 06:55 [entrez]
PHST- 2024/03/20 00:00 [pmc-release]
AID - GLIA24474 [pii]
AID - 10.1002/glia.24474 [doi]
PST - ppublish
SO  - Glia. 2024 Mar;72(3):475-503. doi: 10.1002/glia.24474. Epub 2023 Nov 1.