Evidence map›Paper›PMID 36979408›Full record

ArticleBiomolecules2023

Importance of ACE2 for SARS-CoV-2 Infection of Kidney Cells.

Marie-Kristin Kroll, Sebastian Schloer, Peynaz Candan, Nadia Korthals, Christoph Wenzel, Hannah Ihle, Kevin Gilhaus, Kim Rouven Liedtke, Michael Schöfbänker, Beate Surmann and 8 more

Open access · goldFull text read
In one paragraph

Article in Biomolecules, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Interactions of SARS-CoV-2 with Human Target Cells-A Metabolic View.International journal of molecular sciences · 2024
    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

18 authors at 6 institutions in 1 country.

Marie-Kristin KrollMedizinische Klinik D, Universitätsklinikum Münster, 48149 Münster, Germany.
Sebastian SchloerResearch Group Regulatory Mechanisms of Inflammation, Institute of Medical Biochemistry, Centre for Molecular Biology of Inflammation, University of Münster, 48149 Münster, Germany.
Peynaz CandanResearch Group Regulatory Mechanisms of Inflammation, Institute of Medical Biochemistry, Centre for Molecular Biology of Inflammation, University of Münster, 48149 Münster, Germany.
Nadia KorthalsResearch Group Regulatory Mechanisms of Inflammation, Institute of Medical Biochemistry, Centre for Molecular Biology of Inflammation, University of Münster, 48149 Münster, Germany.
Christoph WenzelInstitut für Pharmakologie, Universitätsmedizin Greifswald, 17489 Greifswald, Germany.ORCID 0000-0002-4361-7575
Hannah IhleInstitute of Forensic Medicine, University Hospital Jena, 07747 Jena, Germany.
Kevin GilhausMedizinische Klinik D, Universitätsklinikum Münster, 48149 Münster, Germany.
Kim Rouven LiedtkeDepartment of General, Visceral, Thoracic and Vascular Surgery, Greifswald University Medical Center, 17475 Greifswald, Germany.ORCID 0000-0002-0273-509X
Michael SchöfbänkerInstitute of Virology (IVM), Center for Molecular Biology of Inflammation (ZMBE), University Hospital Münster, University of Münster, 48149 Münster, Germany.ORCID 0000-0002-3064-4152
Beate SurmannMedizinische Klinik D, Universitätsklinikum Münster, 48149 Münster, Germany.
Rita SchröterMedizinische Klinik D, Universitätsklinikum Münster, 48149 Münster, Germany.
Ute NeugebauerMedizinische Klinik D, Universitätsklinikum Münster, 48149 Münster, Germany.
Gita MallInstitute of Forensic Medicine, University Hospital Jena, 07747 Jena, Germany.
Stefan OswaldInstitut für Pharmakologie und Toxikologie, Universitätsmedizin Rostock, 18057 Rostock, Germany.
Stephan LudwigInstitute of Virology (IVM), Center for Molecular Biology of Inflammation (ZMBE), University Hospital Münster, University of Münster, 48149 Münster, Germany.ORCID 0000-0003-4490-3052
Ursula RescherResearch Group Regulatory Mechanisms of Inflammation, Institute of Medical Biochemistry, Centre for Molecular Biology of Inflammation, University of Münster, 48149 Münster, Germany.ORCID 0000-0001-8892-319X
Beate VollenbrökerMedizinische Klinik D, Universitätsklinikum Münster, 48149 Münster, Germany.ORCID 0000-0001-5259-9017
Giuliano CiarimboliMedizinische Klinik D, Universitätsklinikum Münster, 48149 Münster, Germany.ORCID 0000-0002-4365-3656
University Hospital Münster · DEUniversity of Münster · DEJena University Hospital · DEUniversitätsmedizin Greifswald · DELeibniz Institute of Virology (LIV) · DEUniversitätsmedizin Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In late 2019, the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) as the causative agent of coronavirus disease 2019 (COVID-19) emerged in China and spread rapidly around the world, causing an ongoing pandemic of global concern. COVID-19 proceeds with moderate symptoms in most patients, whereas others experience serious respiratory illness that requires intensive care treatment and may end in death. The severity of COVID-19 is linked to several risk factors including male sex, comorbidities, and advanced age. Apart from respiratory complications, further impairments by COVID-19 affecting other tissues of the human body are observed. In this respect, the human kidney is one of the most frequently affected extrapulmonary organs and acute kidney injury (AKI) is known as a direct or indirect complication of SARS-CoV-2 infection. The aim of this work was to investigate the importance of the protein angiotensin-converting enzyme 2 (ACE2) for a possible cell entry of SARS-CoV-2 into human kidney cells. First, the expression of the cellular receptor ACE2 was demonstrated to be decisive for viral SARS-CoV-2 cell entry in human AB8 podocytes, whereas the presence of the transmembrane protease serine 2 (TMPRSS2) was dispensable. Moreover, the ACE2 protein amount was well detectable by mass spectrometry analysis in human kidneys, while TMPRSS2 could be detected only in a few samples. Additionally, a negative correlation of the ACE2 protein abundance to male sex and elderly aged females in human kidney tissues was demonstrated in this work. Last, the possibility of a direct infection of kidney tubular renal structures by SARS-CoV-2 was demonstrated.

Indexed as

COVID-19AgedAngiotensin-Converting Enzyme 2FemaleHumansKidneyMalePeptidyl-Dipeptidase ASARS-CoV-2ACE2 protein, humanAngiotensin-Converting Enzyme 2Peptidyl-Dipeptidase AACE2kidneysSARS-CoV-2

Identifiers

PMID36979408
PMCPMC10046276
OpenAlexW4323318824

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read66
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.