Evidence map›Paper›PMID 33215884›Full record

Observational studyESC heart failure2021

Decreased GLUT1/NHE1 RNA expression in whole blood predicts disease severity in patients with COVID-19.

Julian Mustroph, Julian Hupf, Frank Hanses, Katja Evert, Maria J Baier, Matthias Evert, Christine Meindl, Stefan Wagner, Ute Hubauer, Gabriela Pietrzyk and 8 more

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in ESC heart failure, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
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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

18 authors at 3 institutions in 2 countries.

Julian MustrophDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
Julian HupfEmergency Department, University Hospital Regensburg, Regensburg, Germany.
Frank HansesEmergency Department, University Hospital Regensburg, Regensburg, Germany.
Katja EvertInstitute of Pathology, University Hospital Regensburg, Regensburg, Germany.
Maria J BaierDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
Matthias EvertInstitute of Pathology, University Hospital Regensburg, Regensburg, Germany.
Christine MeindlDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
Stefan WagnerDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
Ute HubauerDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
Gabriela PietrzykDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
Simon LeiningerDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
Stephan StaudnerDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
Manuel VogelDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
Stefan WallnerDepartment of Clinical Chemistry and Laboratory Medicine, University Hospital Regensburg, Regensburg, Germany.
Markus ZimmermannEmergency Department, University Hospital Regensburg, Regensburg, Germany.
Samuel SossallaDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
Lars S MaierDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
Carsten JungbauerDepartment of Internal Medicine II (Cardiology), University Hospital Regensburg, Franz-Josef-Strauß-Allee 11, Regensburg, 93053, Germany.
University Hospital Regensburg · DEUniversity of Regensburg · DEZero to Three · US

Funding

Deutsche Forschungsgemeinschaft (DFG) 5-1Deutsche Forschungsgemeinschaft (DFG) 7-1Deutsche Forschungsgemeinschaft (DFG) 8-1Deutsche Forschungsgemeinschaft (DFG) Ma1982/5-1Deutsche Forschungsgemeinschaft (DFG) WA 2539/4-1German Cardiac SocietyUniversity of Regensburg SFB 1350 TPA6
6 · The paper itself

Abstract

aimsWe aimed to assess whether expression of whole-blood RNA of sodium proton exchanger 1 (NHE1) and glucose transporter 1 (GLUT1) is associated with COVID-19 infection and outcome in patients presenting to the emergency department with respiratory infections. Furthermore, we investigated NHE1 and GLUT1 expression in the myocardium of deceased COVID-19 patients. METHODS AND

resultsWhole-blood quantitative assessment of NHE1 and GLUT1 RNA was performed using quantitative PCR in patients with respiratory infection upon first contact in the emergency department and subsequently stratified by SARS-CoV-2 infection status. Assessment of NHE1 and GLUT1 RNA using PCR was also performed in left ventricular myocardium of deceased COVID-19 patients. NHE1 expression is up-regulated in whole blood of patients with COVID-19 compared with other respiratory infections at first medical contact in the emergency department (control: 0.0021 ± 0.0002, COVID-19: 0.0031 ± 0.0003, P = 0.01). The ratio of GLUT1 to NHE1 is significantly decreased in the blood of COVID-19 patients who are subsequently intubated and/or die (severe disease) compared with patients with moderate disease (moderate disease: 0.497 ± 0.083 vs. severe disease: 0.294 ± 0.0336, P = 0.036). This ratio is even further decreased in the myocardium of patients who deceased from COVID-19 in comparison with the myocardium of non-infected donors.

conclusionsNHE1 and GLUT1 may be critically involved in the disease progression of SARS-CoV-2 infection. We show here that SARS-CoV-2 infection critically disturbs ion channel expression in the heart. A decreased ratio of GLUT1/NHE1 could potentially serve as a biomarker for disease severity in patients with COVID-19.

Indexed as

Case-Control StudiesCOVID-19Emergency Service, HospitalFemaleGlucose Transporter Type 1HumansMaleMiddle AgedPolymerase Chain ReactionPredictive Value of TestsProspective StudiesRNA, MessengerSeverity of Illness IndexSodium-Hydrogen Exchanger 1Glucose Transporter Type 1RNA, MessengerSLC2A1 protein, humanSLC9A1 protein, humanSodium-Hydrogen Exchanger 1COVID-19GLUT1HeartInfectionNHE1

Identifiers

PMID33215884
PMCPMC7835506
OpenAlexW3099202576

What OpenQuestion holds

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Registered trials

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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.