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1000 Titel
  • Hypoxia-Inducible Factor (HIF) in Ischemic Stroke and Neurodegenerative Disease
1000 Autor/in
  1. Mitroshina, Elena V. |
  2. Savyuk, Maria O. |
  3. Ponimaskin, Evgeni |
  4. Vedunova, Maria V. |
1000 Verlag
  • Frontiers Media S.A.
1000 Erscheinungsjahr 2021
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2021-07-28
1000 Erschienen in
1000 Quellenangabe
  • 9:703084
1000 Copyrightjahr
  • 2021
1000 Embargo
  • 2022-01-30
1000 Lizenz
1000 Verlagsversion
  • https://doi.org/10.3389/fcell.2021.703084 |
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8355741/ |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Abstract/Summary
  • <jats:p>Hypoxia is one of the most common pathological conditions, which can be induced by multiple events, including ischemic injury, trauma, inflammation, tumors, etc. The body’s adaptation to hypoxia is a highly important phenomenon in both health and disease. Most cellular responses to hypoxia are associated with a family of transcription factors called hypoxia-inducible factors (HIFs), which induce the expression of a wide range of genes that help cells adapt to a hypoxic environment. Basic mechanisms of adaptation to hypoxia, and particularly HIF functions, have being extensively studied over recent decades, leading to the 2019 Nobel Prize in Physiology or Medicine. Based on their pivotal physiological importance, HIFs are attracting increasing attention as a new potential target for treating a large number of hypoxia-associated diseases. Most of the experimental work related to HIFs has focused on roles in the liver and kidney. However, increasing evidence clearly demonstrates that HIF-based responses represent an universal adaptation mechanism in all tissue types, including the central nervous system (CNS). In the CNS, HIFs are critically involved in the regulation of neurogenesis, nerve cell differentiation, and neuronal apoptosis. In this mini-review, we provide an overview of the complex role of HIF-1 in the adaptation of neurons and glia cells to hypoxia, with a focus on its potential involvement into various neuronal pathologies and on its possible role as a novel therapeutic target.</jats:p>
1000 Sacherschließung
lokal Alzheimer’s disease
lokal ischemia
lokal HIF
lokal adaptation
lokal Cell and Developmental Biology
lokal hypoxia-inducible factor
lokal neurodegeneration
lokal Parkinson’s disease
lokal hypoxia
1000 Liste der Beteiligten
  1. https://frl.publisso.de/adhoc/uri/TWl0cm9zaGluYSwgRWxlbmEgVi4=|https://frl.publisso.de/adhoc/uri/U2F2eXVrLCBNYXJpYSBPLg==|https://frl.publisso.de/adhoc/uri/UG9uaW1hc2tpbiwgRXZnZW5p|https://frl.publisso.de/adhoc/uri/VmVkdW5vdmEsIE1hcmlhIFYu
1000 Hinweis
  • DeepGreen-ID: 5cf8531d453a4f02ba973af6b40e9696 ; metadata provieded by: DeepGreen (https://www.oa-deepgreen.de/api/v1/), LIVIVO search scope life sciences (http://z3950.zbmed.de:6210/livivo), Crossref Unified Resource API (https://api.crossref.org/swagger-ui/index.html), to.science.api (https://frl.publisso.de/), ZDB JSON-API (beta) (https://zeitschriftendatenbank.de/api/), lobid - Dateninfrastruktur für Bibliotheken (https://lobid.org/resources/search)
1000 Label
1000 Förderer
  1. Ministry of Science and Higher Education of the Russian Federation |
  2. Lobachevsky State University of Nizhny Novgorod |
1000 Fördernummer
  1. -
  2. -
1000 Förderprogramm
  1. -
  2. -
1000 Dateien
1000 Förderung
  1. 1000 joinedFunding-child
    1000 Förderer Ministry of Science and Higher Education of the Russian Federation |
    1000 Förderprogramm -
    1000 Fördernummer -
  2. 1000 joinedFunding-child
    1000 Förderer Lobachevsky State University of Nizhny Novgorod |
    1000 Förderprogramm -
    1000 Fördernummer -
1000 Objektart article
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1000 @id frl:6478493.rdf
1000 Erstellt am 2024-05-21T15:42:53.940+0200
1000 Erstellt von 322
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1000 Zuletzt bearbeitet 2024-05-22T10:59:54.956+0200
1000 Objekt bearb. Wed May 22 10:59:54 CEST 2024
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