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Cells
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Hypoxic-Ischemic Brain Injury: From Molecular Mechanisms to Therapeutic Opportunities
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Hypoxic-Ischemic Brain Injury: From Molecular Mechanisms to Therapeutic Opportunities

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (15 November 2023) | Viewed by 5118

Special Issue Editor

Dr. Eva María Jiménez-Mateos

E-Mail Website
Guest Editor
Trinity College Dublin, Dublin, Ireland
Interests: neuroscience; hypoxia; neonatal; neonatal encephalopathy; hypoxic-ischaemic encephalopathy; microRNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neonatal brain damage or neonatal encephalopathy is mainly caused by hypoxia-ischemia and is a major cause of concern in neonatal units. The prognosis of infants suffering from neonatal brain damage is particularly poor, accounting for 1 million neonatal deaths every year worldwide, and survivors will develop neurological conditions. Both diagnosis and treatment, however, remain a clinical challenge with current therapeutics, being effective only in a subgroup of patients and diagnostic/prognostic methods are either inaccurate or possibly too late for an effective treatment. Since the first preclinical model developed by Rice-Vannuci in rats, new preclinical models have been developed in pigs, sheets, and mice, to mimic the pathology of neonatal encephalopathy in infants. Emerging evidence from these pre-clinical models has started to elucidate the mechanism underlying neonatal brain damage, including oxidative stress, hyperexcitability, and neuroinflammation, which will guide novel therapies and diagnostic tools. This Special Issue will compile the latest results on hypoxia-ischemia encephalopathy.

Dr. Eva María Jiménez-Mateos
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • hypoxia-ischemia
  • encephalopathy
  • brain
  • treatments
  • diagnostics

Published Papers (2 papers)

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Research

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36 pages, 6533 KiB  
Article
Hypothermic Protection in Neocortex Is Topographic and Laminar, Seizure Unmitigating, and Partially Rescues Neurons Depleted of RNA Splicing Protein Rbfox3/NeuN in Neonatal Hypoxic-Ischemic Male Piglets
by Christopher T. Primiani, Jennifer K. Lee, Caitlin E. O’Brien, May W. Chen, Jamie Perin, Ewa Kulikowicz, Polan Santos, Shawn Adams, Bailey Lester, Natalia Rivera-Diaz, Valerie Olberding, Mark V. Niedzwiecki, Eva K. Ritzl, Christa W. Habela, Xiuyun Liu, Zeng-Jin Yang, Raymond C. Koehler and Lee J. Martin
Cells 2023, 12(20), 2454; https://doi.org/10.3390/cells12202454 - 15 Oct 2023
Cited by 1 | Viewed by 1647
Abstract
The effects of hypothermia on neonatal encephalopathy may vary topographically and cytopathologically in the neocortex with manifestations potentially influenced by seizures that alter the severity, distribution, and type of neuropathology. We developed a neonatal piglet survival model of hypoxic-ischemic (HI) encephalopathy and hypothermia [...] Read more.
The effects of hypothermia on neonatal encephalopathy may vary topographically and cytopathologically in the neocortex with manifestations potentially influenced by seizures that alter the severity, distribution, and type of neuropathology. We developed a neonatal piglet survival model of hypoxic-ischemic (HI) encephalopathy and hypothermia (HT) with continuous electroencephalography (cEEG) for seizures. Neonatal male piglets received HI-normothermia (NT), HI-HT, sham-NT, or sham-HT treatments. Randomized unmedicated sham and HI piglets underwent cEEG during recovery. Survival was 2–7 days. Normal and pathological neurons were counted in different neocortical areas, identified by cytoarchitecture and connectomics, using hematoxylin and eosin staining and immunohistochemistry for RNA-binding FOX-1 homolog 3 (Rbfox3/NeuN). Seizure burden was determined. HI-NT piglets had a reduced normal/total neuron ratio and increased ischemic-necrotic/total neuron ratio relative to sham-NT and sham-HT piglets with differing severities in the anterior and posterior motor, somatosensory, and frontal cortices. Neocortical neuropathology was attenuated by HT. HT protection was prominent in layer III of the inferior parietal cortex. Rbfox3 immunoreactivity distinguished cortical neurons as: Rbfox3-positive/normal, Rbfox3-positive/ischemic-necrotic, and Rbfox3-depleted. HI piglets had an increased Rbfox3-depleted/total neuron ratio in layers II and III compared to sham-NT piglets. Neuronal Rbfox3 depletion was partly rescued by HT. Seizure burdens in HI-NT and HI-HT piglets were similar. We conclude that the neonatal HI piglet neocortex has: (1) suprasylvian vulnerability to HI and seizures; (2) a limited neuronal cytopathological repertoire in functionally different regions that engages protective mechanisms with HT; (3) higher seizure burden, insensitive to HT, that is correlated with more panlaminar ischemic-necrotic neurons in the somatosensory cortex; and (4) pathological RNA splicing protein nuclear depletion that is sensitive to HT. This work demonstrates that HT protection of the neocortex in neonatal HI is topographic and laminar, seizure unmitigating, and restores neuronal depletion of RNA splicing factor. Full article
(This article belongs to the Special Issue Hypoxic-Ischemic Brain Injury: From Molecular Mechanisms to Therapeutic Opportunities)
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Review

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18 pages, 1877 KiB  
Review
Hypoxic-Ischemic Brain Injury in ECMO: Pathophysiology, Neuromonitoring, and Therapeutic Opportunities
by Shivalika Khanduja, Jiah Kim, Jin Kook Kang, Cheng-Yuan Feng, Melissa Ann Vogelsong, Romergryko G. Geocadin, Glenn Whitman and Sung-Min Cho
Cells 2023, 12(11), 1546; https://doi.org/10.3390/cells12111546 - 05 Jun 2023
Cited by 2 | Viewed by 3008
Abstract
Extracorporeal membrane oxygenation (ECMO), in conjunction with its life-saving benefits, carries a significant risk of acute brain injury (ABI). Hypoxic-ischemic brain injury (HIBI) is one of the most common types of ABI in ECMO patients. Various risk factors, such as history of hypertension, [...] Read more.
Extracorporeal membrane oxygenation (ECMO), in conjunction with its life-saving benefits, carries a significant risk of acute brain injury (ABI). Hypoxic-ischemic brain injury (HIBI) is one of the most common types of ABI in ECMO patients. Various risk factors, such as history of hypertension, high day 1 lactate level, low pH, cannulation technique, large peri-cannulation PaCO2 drop (∆PaCO2), and early low pulse pressure, have been associated with the development of HIBI in ECMO patients. The pathogenic mechanisms of HIBI in ECMO are complex and multifactorial, attributing to the underlying pathology requiring initiation of ECMO and the risk of HIBI associated with ECMO itself. HIBI is likely to occur in the peri-cannulation or peri-decannulation time secondary to underlying refractory cardiopulmonary failure before or after ECMO. Current therapeutics target pathological mechanisms, cerebral hypoxia and ischemia, by employing targeted temperature management in the case of extracorporeal cardiopulmonary resuscitation (eCPR), and optimizing cerebral O2 saturations and cerebral perfusion. This review describes the pathophysiology, neuromonitoring, and therapeutic techniques to improve neurological outcomes in ECMO patients in order to prevent and minimize the morbidity of HIBI. Further studies aimed at standardizing the most relevant neuromonitoring techniques, optimizing cerebral perfusion, and minimizing the severity of HIBI once it occurs will improve long-term neurological outcomes in ECMO patients. Full article
(This article belongs to the Special Issue Hypoxic-Ischemic Brain Injury: From Molecular Mechanisms to Therapeutic Opportunities)
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