PMID- 32133356
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 2296-634X (Print)
IS  - 2296-634X (Electronic)
IS  - 2296-634X (Linking)
VI  - 8
DP  - 2020
TI  - Current Evidence on Cell Death in Preterm Brain Injury in Human and Preclinical 
      Models.
PG  - 27
LID - 10.3389/fcell.2020.00027 [doi]
LID - 27
AB  - Despite tremendous advances in neonatal intensive care over the past 20 years, 
      prematurity carries a high burden of neurological morbidity lasting lifelong. The 
      term encephalopathy of prematurity (EoP) coined by Volpe in 2009 encompasses all 
      aspects of the now known effects of prematurity on the immature brain, including 
      altered and disturbed development as well as specific lesional hallmarks. 
      Understanding the way cells are damaged is crucial to design brain protective 
      strategies, and in this purpose, preclinical models largely contribute to improve 
      the comprehension of the cell death mechanisms. While neuronal cell death has 
      been deeply investigated and characterized in (hypoxic-ischemic) encephalopathy 
      of the newborn at term, little is known about the types of cell death occurring 
      in preterm brain injury. Three main different morphological cell death types are 
      observed in the immature brain, specifically in models of hypoxic-ischemic 
      encephalopathy, namely, necrotic, apoptotic, and autophagic cell death. Features 
      of all three types may be present in the same dying neuron. In preterm brain 
      injury, description of cell death types is sparse, and cell loss primarily 
      concerns immature oligodendrocytes and, infrequently, neurons. In the present 
      review, we first shortly discuss the different main severe preterm brain injury 
      conditions that have been reported to involve cell death, including 
      periventricular leucomalacia (PVL), diffuse white matter injury (dWMI), and 
      intraventricular hemorrhages, as well as potentially harmful iatrogenic 
      conditions linked to premature birth (anesthesia and caffeine therapy). Then, we 
      present an overview of current evidence concerning cell death in both clinical 
      human tissue data and preclinical models by focusing on studies investigating the 
      presence of cell death allowing discriminating between the types of cell death 
      involved. We conclude that, to improve brain protective strategies, not only 
      apoptosis but also other cell death (such as regulated necrotic and autophagic) 
      pathways now need to be investigated together in order to consider all cell death 
      mechanisms involved in the pathogenesis of preterm brain damage.
CI  - Copyright (c) 2020 Truttmann, Ginet and Puyal.
FAU - Truttmann, Anita C
AU  - Truttmann AC
AD  - Clinic of Neonatology, Department of Women, Mother and Child, University Hospital 
      Center of Vaud, Lausanne, Switzerland.
FAU - Ginet, Vanessa
AU  - Ginet V
AD  - Clinic of Neonatology, Department of Women, Mother and Child, University Hospital 
      Center of Vaud, Lausanne, Switzerland.
AD  - Department of Fundamental Neurosciences, University of Lausanne, Lausanne, 
      Switzerland.
FAU - Puyal, Julien
AU  - Puyal J
AD  - Department of Fundamental Neurosciences, University of Lausanne, Lausanne, 
      Switzerland.
AD  - CURML, University Center of Legal Medicine, Lausanne University Hospital, 
      Lausanne, Switzerland.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20200218
PL  - Switzerland
TA  - Front Cell Dev Biol
JT  - Frontiers in cell and developmental biology
JID - 101630250
PMC - PMC7039819
OTO - NOTNLM
OT  - apoptosis
OT  - autophagic cell death
OT  - autophagy
OT  - necrosis
OT  - neonatal
OT  - neuroprotection
OT  - periventricular leucomalacia
EDAT- 2020/03/07 06:00
MHDA- 2020/03/07 06:01
PMCR- 2020/01/01
CRDT- 2020/03/06 06:00
PHST- 2019/09/13 00:00 [received]
PHST- 2020/01/14 00:00 [accepted]
PHST- 2020/03/06 06:00 [entrez]
PHST- 2020/03/07 06:00 [pubmed]
PHST- 2020/03/07 06:01 [medline]
PHST- 2020/01/01 00:00 [pmc-release]
AID - 10.3389/fcell.2020.00027 [doi]
PST - epublish
SO  - Front Cell Dev Biol. 2020 Feb 18;8:27. doi: 10.3389/fcell.2020.00027. eCollection 
      2020.