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Molecular Advances and Insights into Brain Hypoxia

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 957

Special Issue Editor


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Guest Editor
School of Biomedical Sciences, University of Leeds, Leeds, UK
Interests: brain hypoxia

Special Issue Information

Dear Colleagues,

Brain development and function rely on normal oxygen supply, and its disruption under hypoxia or ischemia is one of the pathological factors leading to neurological disabilities. Restricted oxygen supply to the brain significantly affects cellular functions, with immediate changes in membrane lipids and proteins, as well as long-term changes in gene expression. This can lead to impaired brain development and function in the case of prenatal or neonatal hypoxia and, in later life, can trigger various neurodegenerative disorders, including vascular dementia and Alzheimer’s disease. Acute and chronic brain hypoxia also severly affects the behaviour of individuals and their cognitive abilities, resulting in personality disorders.

In recent years, signficant efforts have been made to understand the molecular mechanisms of hypoxic brain injury, and in 2019, a group of hypoxia researchers (William Kaelin, Sir Peter Ratcliffe and Gregg Semenza) was awarded the Nobel Prize in Physiology or Medicine "for their discoveries of how cells sense and adapt to oxygen availability". The COVID-19 pandemic made it clear that hypoxia is one of the major factors accompanying this lethal disease. Neurological complications have been reported in a large number of COVID-19 patients, adding to the urgency of research relating hypoxia considering there are still limited numbers of new therapeutic targets and approaches to prevent the pathological outcomes of brain hypoxia and ischemia.

This Special Issue welcomes articles and review papers in all areas of hypoxia research, from basic biochemistry (studies in lipids, proteins and nucleic acids), molecular biology (gene expression and regulation), cellular biology (cell death, mitochondria and autophagy), brain morphology (including vascular status and functions of the blood–brain barrier), as well as behavioral and cognitive physiology. Special attention will be paid to the newly developed models and approaches to elucidate endogenous protective mechanisms of hypoxic pre- and postconditioning, and their possible neuroprotective applications.

Dr. Natalia N. Nalivaeva
Guest Editor

Manuscript Submission Information

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Keywords

  • hypoxia
  • ischemia
  • HIF-1
  • COVID-19
  • hypoxic pre- and postconditioning
  • gene expression
  • cell death
  • brain tolerance
  • neurodegeneraion
  • neuroprotection

Published Papers (1 paper)

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Research

19 pages, 4018 KiB  
Article
Metabolite Biomarkers for Early Ischemic–Hypoxic Encephalopathy: An Experimental Study Using the NeoBase 2 MSMS Kit in a Rat Model
by Yulia Shevtsova, Natalia Starodubtseva, Alisa Tokareva, Kirill Goryunov, Alsu Sadekova, Irina Vedikhina, Tatiana Ivanetz, Oleg Ionov, Vladimir Frankevich, Egor Plotnikov, Gennady Sukhikh, Dmitry Zorov and Denis Silachev
Int. J. Mol. Sci. 2024, 25(4), 2035; https://doi.org/10.3390/ijms25042035 - 07 Feb 2024
Viewed by 705
Abstract
Hypoxic–ischemic encephalopathy (HIE) is one of the most common causes of childhood disability. Hypothermic therapy is currently the only approved neuroprotective approach. However, early diagnosis of HIE can be challenging, especially in the first hours after birth when the decision to use hypothermic [...] Read more.
Hypoxic–ischemic encephalopathy (HIE) is one of the most common causes of childhood disability. Hypothermic therapy is currently the only approved neuroprotective approach. However, early diagnosis of HIE can be challenging, especially in the first hours after birth when the decision to use hypothermic therapy is critical. Distinguishing HIE from other neonatal conditions, such as sepsis, becomes a significant problem in diagnosis. This study explored the utility of a metabolomic-based approach employing the NeoBase 2 MSMS kit to diagnose HIE using dry blood stains in a Rice–Vannucci model of HIE in rats. We evaluated the diagnostic fidelity of this approach in a range between 3 and 6 h after the onset of HIE, including in the context of systemic inflammation and concomitant hypothermic therapy. Discriminant analysis revealed several metabolite patterns associated with HIE. A logistic regression model using glycine levels achieved high diagnostic fidelity with areas under the receiver operating characteristic curve of 0.94 at 3 h and 0.96 at 6 h after the onset of HIE. In addition, orthogonal partial least squares discriminant analysis, which included five metabolites, achieved 100% sensitivity and 80% specificity within 3 h of HIE. These results highlight the significant potential of the NeoBase 2 MSMS kit for the early diagnosis of HIE and could improve patient management and outcomes in this serious illness. Full article
(This article belongs to the Special Issue Molecular Advances and Insights into Brain Hypoxia)
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