PMID- 34440681
OWN - NLM
STAT- MEDLINE
DCOM- 20211111
LR  - 20211111
IS  - 2073-4409 (Electronic)
IS  - 2073-4409 (Linking)
VI  - 10
IP  - 8
DP  - 2021 Jul 28
TI  - Cumulative Damage: Cell Death in Posthemorrhagic Hydrocephalus of Prematurity.
LID - 10.3390/cells10081911 [doi]
LID - 1911
AB  - Globally, approximately 11% of all infants are born preterm, prior to 37 weeks' 
      gestation. In these high-risk neonates, encephalopathy of prematurity (EoP) is a 
      major cause of both morbidity and mortality, especially for neonates who are born 
      very preterm (<32 weeks gestation). EoP encompasses numerous types of preterm 
      birth-related brain abnormalities and injuries, and can culminate in a diverse 
      array of neurodevelopmental impairments. Of note, posthemorrhagic hydrocephalus 
      of prematurity (PHHP) can be conceptualized as a severe manifestation of EoP. 
      PHHP impacts the immature neonatal brain at a crucial timepoint during 
      neurodevelopment, and can result in permanent, detrimental consequences to not 
      only cerebrospinal fluid (CSF) dynamics, but also to white and gray matter 
      development. In this review, the relevant literature related to the diverse 
      mechanisms of cell death in the setting of PHHP will be thoroughly discussed. 
      Loss of the epithelial cells of the choroid plexus, ependymal cells and their 
      motile cilia, and cellular structures within the glymphatic system are of 
      particular interest. Greater insights into the injuries, initiating targets, and 
      downstream signaling pathways involved in excess cell death shed light on 
      promising areas for therapeutic intervention. This will bolster current efforts 
      to prevent, mitigate, and reverse the consequential brain remodeling that occurs 
      as a result of hydrocephalus and other components of EoP.
FAU - Sevensky, Riley
AU  - Sevensky R
AD  - Division of Neonatal-Perinatal Medicine, Department of Pediatrics, Johns Hopkins 
      University School of Medicine, Baltimore, MD 21205, USA.
FAU - Newville, Jessie C
AU  - Newville JC
AUID- ORCID: 0000-0002-8590-7968
AD  - Division of Neonatal-Perinatal Medicine, Department of Pediatrics, Johns Hopkins 
      University School of Medicine, Baltimore, MD 21205, USA.
FAU - Tang, Ho Lam
AU  - Tang HL
AD  - Division of Pediatric Neurosurgery, Department of Neurosurgery, Johns Hopkins 
      University School of Medicine, Baltimore, MD 21205, USA.
FAU - Robinson, Shenandoah
AU  - Robinson S
AD  - Division of Pediatric Neurosurgery, Department of Neurosurgery, Johns Hopkins 
      University School of Medicine, Baltimore, MD 21205, USA.
FAU - Jantzie, Lauren L
AU  - Jantzie LL
AD  - Division of Neonatal-Perinatal Medicine, Department of Pediatrics, Johns Hopkins 
      University School of Medicine, Baltimore, MD 21205, USA.
AD  - Division of Pediatric Neurosurgery, Department of Neurosurgery, Johns Hopkins 
      University School of Medicine, Baltimore, MD 21205, USA.
AD  - Department of Neurology and Developmental Medicine, Kennedy Krieger Institute, 
      Baltimore, MD 21205, USA.
AD  - Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, 
      MD 21205, USA.
LA  - eng
GR  - W81XWH-18-1-0166/U.S. Department of Defense/
GR  - W81XWH-18-1-0167/U.S. Department of Defense/
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Review
DEP - 20210728
PL  - Switzerland
TA  - Cells
JT  - Cells
JID - 101600052
SB  - IM
MH  - Brain/growth & development/metabolism/pathology
MH  - *Cell Death
MH  - Choroid Plexus/cytology/metabolism
MH  - Cilia/metabolism
MH  - Ependyma/cytology/metabolism
MH  - Humans
MH  - Hydrocephalus/cerebrospinal fluid/genetics/*pathology
MH  - Infant, Premature, Diseases/cerebrospinal fluid/genetics/*pathology
MH  - Premature Birth
MH  - Signal Transduction
PMC - PMC8393895
OTO - NOTNLM
OT  - cell death
OT  - choroid plexus
OT  - encephalopathy of prematurity
OT  - ependyma
OT  - ferroptosis
OT  - glymphatic system
OT  - hydrocephalus
OT  - inflammation
OT  - neurodevelopment
OT  - preterm birth
COIS- The authors declare no conflict of interest.
EDAT- 2021/08/28 06:00
MHDA- 2021/11/12 06:00
PMCR- 2021/07/28
CRDT- 2021/08/27 01:07
PHST- 2021/06/08 00:00 [received]
PHST- 2021/07/23 00:00 [revised]
PHST- 2021/07/25 00:00 [accepted]
PHST- 2021/08/27 01:07 [entrez]
PHST- 2021/08/28 06:00 [pubmed]
PHST- 2021/11/12 06:00 [medline]
PHST- 2021/07/28 00:00 [pmc-release]
AID - cells10081911 [pii]
AID - cells-10-01911 [pii]
AID - 10.3390/cells10081911 [doi]
PST - epublish
SO  - Cells. 2021 Jul 28;10(8):1911. doi: 10.3390/cells10081911.