ArticleBulletin of experimental biology and medicine2022
Regulation and Role of Hypoxia-Induced Factor 1α (HIF-1α) under Conditions of Endogenous Oxidative Stress In Vitro.
Article in Bulletin of experimental biology and medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Hypoxic Natural Killer Cells-Derived HIF-1α-Containing Exosomes Inhibit Cellular Senescence and Apoptosis in Neurocytes to Ameliorate Alzheimer's Disease by Eliminating Oxidative Damages.Molecular neurobiology · 2025Article
- Ferulic Acid Methyl Ester Attenuates Cerebral Ischemia-Reperfusion Injury in Rats by Modulating PI3K/HIF-1α/VEGF Signaling Pathway.Journal of inflammation research · 2024Article
- Glutathione Depletion Disrupts Redox Homeostasis in an Anoxia-Tolerant Invertebrate.Antioxidants (Basel, Switzerland) · 2023Article
- Mechanisms of P-Glycoprotein Regulation Under Exogenous and Endogenous Oxidative Stress In Vitro.Acta naturaeArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of endogenous oxidative stress induced by γ-glutamyl cysteinesynthetase inhibitor D,L-buthionine sulfoximine (BSO) on the functioning of hypoxia-induced factor 1α (HIF-1α) was studied on Caco-2 cells. BSO was added for 24 h in concentrations of 5, 10, 50, 100, and 500 μM. It was shown that BSO in concentrations of 10, 50, and 100 μM induced endogenous oxidative stress and increased the content of HIF-1α; this effect was regulated through nuclear factor of erythroid origin 2 (Nrf2). Activation of HIF-1α had an independent protective effect, as evidenced by the decrease in cell viability after HIF-1α inhibition under these conditions. When the concentration of BSO was increased to 500 μM the content of HIF-1α did not change, and cell viability decreased.
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