Regular ArticlesCerebral white matter damage in the preterm infant: pathophysiology and risk factors
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Cited by (79)
Profiling analysis reveals the potential contribution of long non-coding RNAs to preterm white matter injury
2020, Life SciencesCitation Excerpt :Combined with the results of recent studies of preterm WMI, the following pathways were considered strong candidates for further research: the VEGF signaling pathway, natural killer cell-mediated cytotoxicity pathway, apoptotic signaling pathway, and autophagy pathway. Premature infants are particularly vulnerable to injury owing to incomplete brain development, with especially poor circulatory adaptation [23]. VEGF plays an important role in neovascularization by protecting neurons and glia.
Cell-based strategies to reconstitute vital functions in preterm infants with organ failure
2016, Best Practice and Research: Clinical Obstetrics and GynaecologyCitation Excerpt :The posthemorrhagic ventricular dilatation is attributed to inflammation in the subarachnoid spaces induced by contact with blood products, leading to obstructive arachnoiditis and reduced cerebrospinal fluid (CSF) resorption [74]. Moreover, pro-inflammatory cytokines originating from blood products in the cerebral ventricles may further aggravate injury to the periventricular WMI; therefore, new therapies with potent anti-inflammatory actions may be of great value in preventing brain damage and posthemorrhagic hydrocephalus after severe IVH [75]. This has also been demonstrated by Ahn et al. in a newborn rat model of IVH, where the intraventricular administration of UC-derived MSCs on postnatal day 4 was able to prevent posthemorrhagic hydrocephalus development and also significantly attenuate impairment on behavioral tests.
Oligodendrocyte Progenitor Cell Transplantation Ameliorates Preterm Infant Cerebral White Matter Injury in Rats Model
2023, Neuropsychiatric Disease and Treatment
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Correspondence to Elie Saliba, INSERM U 316, Department of Neonatology, Hôpital Clocheville, 49, Bd Béranger F-37000, France. E-mail:[email protected]