Evidence map›Paper›PMID 33444904›Full record

ArticleMedical hypotheses2021

COVID-19 patients may become predisposed to pulmonary arterial hypertension.

Yuichiro J Suzuki, Sofia I Nikolaienko, Nataliia V Shults, Sergiy G Gychka

Open access · hybridAbstract read
In one paragraph

Article in Medical hypotheses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Mechanisms of lung endothelial cell injury and survival in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024
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  14. Molecular Pathways in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Review
  17. Mechanisms of pulmonary vascular dysfunction in pulmonary hypertension and implications for novel therapies.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  18. Review
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  20. Review
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

4 authors at 3 institutions in 2 countries.

Yuichiro J SuzukiDepartment of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20007, USA. Electronic address: ys82@georgetown.edu.
Sofia I NikolaienkoDepartment of Pathological Anatomy N2, Bogomolets National Medical University, Kyiv 01601, Ukraine.
Nataliia V ShultsDepartment of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20007, USA.
Sergiy G GychkaDepartment of Pathological Anatomy N2, Bogomolets National Medical University, Kyiv 01601, Ukraine.
Bogomolets National Medical University · UAGeorgetown University · USGeorgetown University Medical Center · US

Funding

New mechanism of cellular protein oxidationR21AI142649 · NIAID · GEORGETOWN UNIVERSITY · PI SUZUKI, YUICHIRO JUSTIN · 2019 to 2020
$428k
Oxidant-mediated amino acid conversions in alcohol abuseR03AA026516 · NIAAA · GEORGETOWN UNIVERSITY · PI SUZUKI, YUICHIRO JUSTIN · 2019 to 2020
$156k
Endogenous protein engineering mechanismof oxidative stress in Alzheimer's diseaseR03AG059554 · NIA · GEORGETOWN UNIVERSITY · PI SUZUKI, YUICHIRO JUSTIN · 2018 to 2019
$156k
NIAAA NIH HHS R03 AA026516NIAID NIH HHS R21 AI142649NIA NIH HHS R03 AG059554
6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing the current pandemic of coronavirus disease 2019 (COVID-19) that have killed over one million people worldwide so far. To date, over forty million people have officially been identified to be infected with this virus with less than 3% death rate. Since many more people are expected to have been infected with this virus without the official diagnosis, the number of people who have recovered from the SARS-CoV-2 infection should be substantial. Given the large number of people recovered from either the mild SARS-CoV-2 infection or more severe COVID-19 conditions, it is critical to understand the long-term consequences of the infection by this virus. Our histological evaluations revealed that patients died of COVID-19 exhibited thickened pulmonary vascular walls, one important hallmark of pulmonary arterial hypertension (PAH). By contrast, such pulmonary vascular remodeling lesions were not found in patients died of SARS-CoV-1 during the 2002-2004 SARS outbreak or due to the infection by H1N1 influenza. The advancement in the treatment for the human immunodeficiency virus (HIV) infection has been remarkable that HIV-infected individuals now live for a long time, in turn revealing that these individuals become susceptible to developing PAH, a fatal condition. We herein hypothesize that SARS-CoV-2 is another virus that is capable to triggering the increased susceptibility of infected individuals to developing PAH in the future. Given the large number of people being infected with SARS-CoV-2 during this pandemic and that most people recover from severe, mild or asymptomatic conditions, it is imperative to generate scientific information on how the health of recovered individuals may be affected long-term. PAH is one lethal consequence that should be considered and needs to be monitored. This may also foster the research on developing therapeutic agents to prevent PAH, which has not so far been successful.

Indexed as

AnimalsComorbidityCOVID-19Disease OutbreaksDisease SusceptibilityEndothelium, VascularHumansInfluenza A Virus, H1N1 SubtypeInfluenza, HumanLungModels, TheoreticalPulmonary Arterial HypertensionUkraine

Identifiers

PMID33444904
PMCPMC7787059
OpenAlexW3118609351

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.