Evidence map›Paper›PMID 34440358›Full record

ArticleGenes2021

MiRNA Let-7a and Let-7d Are Induced by Globotriaosylceramide via NF-kB Activation in Fabry Disease.

Nadine Maier, Constantin Gatterer, Patrick Haider, Manuel Salzmann, Christoph Kaun, Walter S Speidl, Gere Sunder-Plassmann, Bruno K Podesser, Johann Wojta, Senta Graf and 2 more

Open access · goldAbstract read
In one paragraph

Article in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Mitochondrial microRNAs Are Dysregulated in Patients with Fabry Disease.The Journal of pharmacology and experimental therapeutics · 2023
    Article
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

12 authors at 2 institutions in 1 country.

Nadine MaierDepartment of Internal Medicine II/Cardiology, Medical University of Vienna, 1090 Vienna, Austria.
Constantin GattererDepartment of Internal Medicine II/Cardiology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-1029-085X
Patrick HaiderDepartment of Internal Medicine II/Cardiology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0001-6874-5349
Manuel SalzmannDepartment of Internal Medicine II/Cardiology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0001-5477-3533
Christoph KaunDepartment of Internal Medicine II/Cardiology, Medical University of Vienna, 1090 Vienna, Austria.
Walter S SpeidlDepartment of Internal Medicine II/Cardiology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-7267-3138
Gere Sunder-PlassmannDepartment of Internal Medicine III/Nephrology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-9253-9921
Bruno K PodesserCenter for Biomedical Research, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-4641-7202
Johann WojtaDepartment of Internal Medicine II/Cardiology, Medical University of Vienna, 1090 Vienna, Austria.
Senta GrafDepartment of Internal Medicine II/Cardiology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-4443-8667
Max LenzDepartment of Internal Medicine II/Cardiology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-3539-994X
Philipp J HohensinnerDepartment of Internal Medicine II/Cardiology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-4819-3190
Medical University of Vienna · ATLudwig Boltzmann Institute for Cancer Research · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFabry disease is a hereditary genetic defect resulting in reduced activity of the enzyme α-galactosidase-A and the accumulation of globotriaosylceramide (Gb3) in body fluids and cells. Gb3 accumulation was especially reported for the vascular endothelium in several organs.

methodsThree Fabry disease patients were screened using a micro-RNA screen. An in vitro approach in human endothelial cells was used to determine miRNA regulation by Gb3.

resultsIn a micro-RNA screen of three Fabry patients undergoing enzyme replacement therapy, we found that miRNAs let-7a and let-7d were significantly increased after therapy. We demonstrate in vitro in endothelial cells that Gb3 induced activation of NF-κB and activated downstream targets. In addition, NF-κB activity directly reduced let-7a and let-7d miRNA expression as inhibiting NF-kB nuclear entry abolished the Gb3 effects.

conclusionWe suggest that let-7a and let-7d are potential markers for enzyme activity and inflammation in Fabry disease patients.

Indexed as

AdultCells, CulturedEndothelial CellsEnzyme Replacement TherapyFabry DiseaseFemaleGene Expression RegulationHumansMaleMicroRNAsMiddle AgedNF-kappa BTrihexosylceramidesglobotriaosylceramideMicroRNAsmirnlet7 microRNA, humanNF-kappa BTrihexosylceramidesFabry diseaseGb3inflammationNF-κB

Identifiers

PMID34440358
PMCPMC8394417
OpenAlexW3186255320

What OpenQuestion 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 OpenQuestion graph.