Evidence map›Paper›PMID 35110370›Full record

ArticleLife science alliance2022

Proteomic landscape of SARS-CoV-2- and MERS-CoV-infected primary human renal epithelial cells.

Aneesha Kohli, Lucie Sauerhering, Sarah K Fehling, Kevin Klann, Helmut Geiger, Stephan Becker, Benjamin Koch, Patrick C Baer, Thomas Strecker, Christian Münch

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

5 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Choosing a cellular model to study SARS-CoV-2.Frontiers in cellular and infection microbiology · 2022
    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

10 authors at 2 institutions in 1 country.

Aneesha KohliInstitute of Biochemistry II, Faculty of Medicine, Goethe University, Frankfurt am Main, Germany.
Lucie SauerheringInstitute of Virology, Philipps University Marburg, Marburg, Germany.
Sarah K FehlingInstitute of Virology, Philipps University Marburg, Marburg, Germany.
Kevin KlannInstitute of Biochemistry II, Faculty of Medicine, Goethe University, Frankfurt am Main, Germany.
Helmut GeigerDivision of Nephrology, Department of Internal Medicine III, University Hospital, Goethe-University, Frankfurt am Main, Germany.
Stephan BeckerInstitute of Virology, Philipps University Marburg, Marburg, Germany.
Benjamin KochDivision of Nephrology, Department of Internal Medicine III, University Hospital, Goethe-University, Frankfurt am Main, Germany.
Patrick C BaerDivision of Nephrology, Department of Internal Medicine III, University Hospital, Goethe-University, Frankfurt am Main, Germany p.baer@em.uni-frankfurt.de.ORCID 0000-0001-8113-3312
Thomas StreckerInstitute of Virology, Philipps University Marburg, Marburg, Germany strecker@staff.uni-marburg.de.ORCID 0000-0002-7857-937X
Christian MünchInstitute of Biochemistry II, Faculty of Medicine, Goethe University, Frankfurt am Main, Germany ch.muench@em.uni-frankfurt.de.ORCID 0000-0003-3832-090X
Goethe University Frankfurt · DEPhilipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury is associated with mortality in COVID-19 patients. However, host cell changes underlying infection of renal cells with SARS-CoV-2 remain unknown and prevent understanding of the molecular mechanisms that may contribute to renal pathology. Here, we carried out quantitative translatome and whole-cell proteomics analyses of primary renal proximal and distal tubular epithelial cells derived from human donors infected with SARS-CoV-2 or MERS-CoV to disseminate virus and cell type-specific changes over time. Our findings revealed shared pathways modified upon infection with both viruses, as well as SARS-CoV-2-specific host cell modulation driving key changes in innate immune activation and cellular protein quality control. Notably, MERS-CoV infection-induced specific changes in mitochondrial biology that were not observed in response to SARS-CoV-2 infection. Furthermore, we identified extensive modulation in pathways associated with kidney failure that changed in a virus- and cell type-specific manner. In summary, we provide an overview of the effects of SARS-CoV-2 or MERS-CoV infection on primary renal epithelial cells revealing key pathways that may be essential for viral replication.

Indexed as

KidneyProteomeProteomicsBiomarkersCell NucleusCells, CulturedComputational BiologyCOVID-19Epithelial CellsGene Expression RegulationHost-Pathogen InteractionsHumansKidney Tubules, DistalKidney Tubules, ProximalMiddle East Respiratory Syndrome CoronavirusMitochondriaBiomarkersProteome

Identifiers

PMID35110370
PMCPMC8814637
OpenAlexW4210598918

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.