Evidence map›Paper›PMID 33110240›Full record

ReviewActa pharmacologica Sinica2020

Hypoxia, HIF-1α, and COVID-19: from pathogenic factors to potential therapeutic targets.

Zoya O Serebrovska, Elisa Y Chong, Tetiana V Serebrovska, Lesia V Tumanovska, Lei Xi

Open access · bronzeAbstract readReview
In one paragraph

Review in Acta pharmacologica Sinica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 3 pooled it
4.1field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

123 citing papers in PubMed, 3 syntheses or guidelines pooled it, 216 citations in OpenAlex.

  1. Pooled it
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  3. Neuropathologic findings of patients with COVID-19: a systematic review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Pooled it
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  19. Classification and regulatory interactions of key transcription factors in COVID-19.Frontiers in cellular and infection microbiology · 2025
    Review
  20. Nature's cryptographic codebreakerFrontiers in microbiology · 2025
    Article

63 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 2 countries.

Zoya O SerebrovskaBogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, 01024, Ukraine. belyak-serebrovska@hotmail.com.
Elisa Y ChongDepartment of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA, 02114, USA.
Tetiana V SerebrovskaBogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, 01024, Ukraine.
Lesia V TumanovskaBogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kiev, 01024, Ukraine.
Lei XiPauley Heart Center, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, 23298-0204, USA. lei.xi@vcuhealth.org.
National Academy of Sciences of Ukraine · UABogomoletz Institute of Physiology · UAMassachusetts General Hospital · USVirginia Commonwealth University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pandemic of coronavirus disease 2019 (COVID-19) and its pathogen, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have become the greatest current threat to global public health. The highly infectious SARS-CoV-2 virus primarily attacks pulmonary tissues and impairs gas exchange leading to acute respiratory distress syndrome (ARDS) and systemic hypoxia. The current pharmacotherapies for COVID-19 largely rely on supportive and anti-thrombi treatment and the repurposing of antimalarial and antiviral drugs such as hydroxychloroquine and remdesivir. For a better mechanistic understanding of COVID-19, our present review focuses on its primary pathophysiologic features: hypoxia and cytokine storm, which are a prelude to multiple organ failure and lethality. We discussed a possible link between the activation of hypoxia inducible factor 1α (HIF-1α) and cell entry of SARS-CoV-2, since HIF-1α is shown to suppress the angiotensin-converting enzyme 2 (ACE2) receptor and transmembrane protease serine 2 (TMPRSS2) and upregulate disintegrin and metalloproteinase domain-containing protein 17 (ADAM17). In addition, the protein targets of HIF-1α are involved with the activation of pro-inflammatory cytokine expression and the subsequent inflammatory process. Furthermore, we hypothesized a potential utility of so-called "hypoxic conditioning" to activate HIF-1α-induced cytoprotective signaling for reduction of illness severity and improvement of vital organ function in patients with COVID-19. Taken together, we would propose further investigations into the hypoxia-related molecular mechanisms, from which novel targeted therapies can be developed for the improved management of COVID-19.

Indexed as

COVID-19 Drug TreatmentAnimalsAntiviral AgentsCOVID-19Cytokine Release SyndromeDrug DevelopmentDrug RepositioningHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMolecular Targeted TherapySARS-CoV-2Antiviral AgentsHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitACE2COVID-19cytokineHIF-1αhypoxiahypoxic conditioning

Identifiers

PMID33110240
PMCPMC7588589
OpenAlexW3095842354

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.