Evidence map›Paper›PMID 34392451›Full record

ReviewMolecular biology reports2021

How SARS-CoV-2 might affect potassium balance via impairing epithelial sodium channels?

Maryam Noori, Seyed Aria Nejadghaderi, Mark J M Sullman, Kristin Carson-Chahhoud, Mohammadreza Ardalan, Ali-Asghar Kolahi, Saeid Safiri

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

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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

7 authors at 6 institutions in 3 countries.

Maryam NooriStudent Research Committee, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Seyed Aria NejadghaderiSchool of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mark J M SullmanDepartment of Social Sciences, University of Nicosia, Nicosia, Cyprus.
Kristin Carson-ChahhoudAustralian Centre for Precision Health, University of South Australia, Adelaide, Australia.
Mohammadreza ArdalanKidney Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Ali-Asghar KolahiSocial Determinants of Health Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. a.kolahi@sbmu.ac.ir.
Saeid SafiriTuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. safiris@tbzmed.ac.ir.ORCID http://orcid.org/0000-0001-7986-9072
Tabriz University of Medical Sciences · IRIran University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IRUniversal Scientific Education and Research Network · IRUniversity of Nicosia · CYUniversity of South Australia · AU

Funding

shahid beheshti university of medical sciences 24495
6 · The paper itself

Abstract

Severe acute respiratory syndrome coronaviruses 2 (SARS-CoV-2) is the causative agent of current coronavirus disease 2019 (COVID-19) pandemic. Electrolyte disorders particularly potassium abnormalities have been repeatedly reported as common clinical manifestations of COVID-19. Here, we discuss how SARS-CoV-2 may affect potassium balance by impairing the activity of epithelial sodium channels (ENaC). The first hypothesis could justify the incidence of hypokalemia. SARS-CoV-2 cell entry through angiotensin-converting enzyme 2 (ACE2) may enhance the activity of renin-angiotensin-aldosterone system (RAAS) classical axis and further leading to over production of aldosterone. Aldosterone is capable of enhancing the activity of ENaC and resulting in potassium loss from epithelial cells. However, type II transmembrane serine protease (TMPRSS2) is able to inhibit the ENaC, but it is utilized in the case of SARS-CoV-2 cell entry, therefore the ENaC remains activated. The second hypothesis describe the incidence of hyperkalemia based on the key role of furin. Furin is necessary for cleaving both SARS-CoV-2 spike protein and ENaC subunits. While the furin is hijacked by the virus, the decreased activity of ENaC would be expected, which causes retention of potassium ions and hyperkalemia. Given that the occurrence of hypokalemia is higher than hyperkalemia in COVID-19 patients, the first hypothesis may have greater impact on potassium levels. Further investigations are warranted to determine the exact role of ENaC in SARS-CoV-2 pathogenesis.

Indexed as

COVID-19Epithelial CellsEpithelial Sodium ChannelsFurinHumansPandemicsPotassiumSARS-CoV-2Serine EndopeptidasesSpike Glycoprotein, CoronavirusEpithelial Sodium ChannelsFurinPotassiumSerine EndopeptidasesSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-22019-nCoVCOVID-19ElectrolytesENaCEpithelial sodium channelsHyperkalemiaHypokalemiaSARS-CoV-2Serum potassium

Identifiers

PMID34392451
PMCPMC8364628
OpenAlexW3195131321

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.