Evidence map›Paper›PMID 32504923›Full record

ArticleMedical hypotheses2020

N-Acetylcysteine: A potential therapeutic agent for SARS-CoV-2.

Francis L Poe, Joshua Corn

Open access · greenAbstract read
In one paragraph

Article in Medical hypotheses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
3.1field-weighted citation impact, top 5% 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

68 citing papers in PubMed, 132 citations in OpenAlex.

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8 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

2 authors at 1 institution in 1 country.

Francis L PoeWhole Systems Research Institute, 1020 SW Taylor St Ste. 340, Portland, OR 97239, United States. Electronic address: lpoe@wshcare.org.
Joshua CornWhole Systems Research Institute, 1020 SW Taylor St Ste. 340, Portland, OR 97239, United States.
Oregon Research Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COVID-19, a respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), continues to spread across the globe. Predisposing factors such as age, diabetes, cardiovascular disease, and lowered immune function increase the risk of disease severity. T cell exhaustion, high viral load, and high levels of TNF-ɑ, IL1β, IL6, IL10 have been associated with severe SARS-CoV-2. Cytokine and antigen overstimulation are potentially responsible for poor humoral response to the virus. Lower cellular redox status, which leads to pro-inflammatory states mediated by TNF-ɑ is also potentially implicated. In vivo, in vitro, and human clinical trials have demonstrated N-acetylcysteine (NAC) as an effective method of improving redox status, especially when under oxidative stress. In human clinical trials, NAC has been used to replenish glutathione stores and increase the proliferative response of T cells. NAC has also been shown to inhibit the NLRP3 inflammasome pathway (IL1β and IL18) in vitro, and decrease plasma TNF-ɑ in human clinical trials. Mediation of the viral load could occur through NAC's ability to increase cellular redox status via maximizing the rate limiting step of glutathione synthesis, and thereby potentially decreasing the effects of virally induced oxidative stress and cell death. We hypothesize that NAC could act as a potential therapeutic agent in the treatment of COVID-19 through a variety of potential mechanisms, including increasing glutathione, improving T cell response, and modulating inflammation. In this article, we present evidence to support the use of NAC as a potential therapeutic agent in the treatment of COVID-19.

Indexed as

AcetylcysteineBetacoronavirusClinical Trials as TopicCoronavirus InfectionsCOVID-19COVID-19 Drug TreatmentFree RadicalsGlutathioneHumansInflammationNLR Family, Pyrin Domain-Containing 3 ProteinOxidation-ReductionOxidative StressPandemicsPneumonia, ViralSARS-CoV-2AcetylcysteineFree RadicalsGlutathioneNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanTNF protein, humanTumor Necrosis Factor-alphaCoronavirusCOVID-19GlutathioneNACN-acetylcysteineNLRP3Oxidative stressRedox potentialRedox statusSARS-COV-2T Cell ExhaustionTNF-ɑ

Identifiers

PMID32504923
PMCPMC7261085
OpenAlexW3030752164

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.