ArticleScientific reports2019
Transcription Factors Regulation in Human Peripheral White Blood Cells during Hypobaric Hypoxia Exposure: an in-vivo experimental study.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Systematic review and meta-analysis of antioxidant treatment in patients with acute mountain sickness induced by high altitude exposure.Frontiers in physiology · 2026Pooled it
- Acclimatization Effects ofInternational journal of molecular sciences · 2026Article
- Myeloperoxidase regulates hypoxia-induced inflammation and oxidative stress in liver-spleen axis.Journal of inflammation (London, England) · 2026Article
- Mechanisms underlying end-organ injury in sleep apnoea.The European respiratory journal · 2026Review
- Altitude hypoxia and hypoxemia: pathogenesis and management.Signal transduction and targeted therapy · 2026Review
- Low hypoxia tolerance as a determinant of the proinflammatory phenotype: a trained immunity perspective.Frontiers in immunology · 2026Review
- Gut-heart axis at high altitude: a dynamic mediator from hypoxic dysbiosis to adaptive cardioprotection.Frontiers in microbiology · 2026Review
- Elevated Red Cell Distribution Width as a Potential Marker of Acute Mountain Sickness in Chinese Young Men Upon Rapidly Ascending to 3,650 m.International journal of general medicine · 2026Article
- Demographics, cardiopulmonary comorbidities, laboratory data and length of hospital stay in patients with acute exacerbation of chronic obstructive pulmonary disease at high altitude: A comparative study.Experimental and therapeutic medicine · 2025Article
- Dysregulation of metabolites and high-altitude illnesses development under plateau conditions.Frontiers in physiology · 2025Review
- Wharton's jelly-derived mesenchymal stem cells ameliorate high altitude-induced heart injury by promoting type 2 macrophage polarization via COX2-PGE2 pathway.Frontiers in immunology · 2025Article
- Review
- Research Progress on Using Nanoparticles to Enhance the Efficacy of Drug Therapy for Chronic Mountain Sickness.Pharmaceutics · 2024Review
- Decompression Illness After Technical Diving Session in Mediterranean Sea: Oxidative Stress, Inflammation, and HBO Therapy.International journal of molecular sciences · 2024Article
- Network pharmacology andHeliyon · 2024Article
- Nitronyl Nitroxide Ameliorates Hypobaric Hypoxia-Induced Cognitive Impairment in Mice by Suppressing the Oxidative Stress, Inflammatory Response and Apoptosis.Neurochemical research · 2024Article
- Transcriptomic signatures of severe acute mountain sickness during rapid ascent to 4,300 m.Frontiers in physiology · 2024Article
- Endocrine, inflammatory and immune responses and individual differences in acute hypobaric hypoxia in lowlanders.Scientific reports · 2023Article
- A Tale of Two: When Neural Stem Cells Encounter Hypoxia.Cellular and molecular neurobiology · 2023Review
- The "ON-OFF" Switching Response of Reactive Oxygen Species in Acute Normobaric Hypoxia: Preliminary Outcome.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High altitude is a natural laboratory, within which the clinical study of human physiological response to hypobaric hypoxia (HH) is possible. Failure in the response results in progressive hypoxemia, inflammation and increased tissue oxidative stress (OxS). Thus, investigating temporal changes in key transcription factors (TFs) HIF-1α, HIF-2α, NF-κB and NRF2 mRNA levels, relative to OxS and inflammatory markers, may reveal molecular targets which contrast deleterious effects of hypoxia. Biological samples and clinical data from 15 healthy participants were collected at baseline and after rapid, passive ascent to 3830 m (24 h and 72 h). Gene expression was assessed by qPCR and ROS generation was determined by EPR spectroscopy. Oxidative damage and cytokine levels were estimated by immuno or enzymatic methods. Hypoxia transiently enhanced HIF-1α mRNA levels over time reaching a peak after 24 h. Whereas, HIF-2α and NRF2 mRNA levels increased over time. In contrast, the NF-κB mRNA levels remained unchanged. Plasma levels of IL-1β and IL-6 also remained within normal ranges. ROS production rate and markers of OxS damage were significantly increased over time. The analysis of TF-gene expression suggests that HIF-1α is a lead TF during sub-acute HH exposure. The prolongation of the HH exposure led to a switch between HIF-1α and HIF-2α/NRF2, suggesting the activation of new pathways. These results provide new insights regarding the temporal regulation of TFs, inflammatory state, and ROS homeostasis involved in human hypoxic response, potentially also relevant to the mediation of diseases that induce a hypoxic state.
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