Evidence map›Paper›PMID 31766264›Full record

ArticleBiomolecules2019

Retinol Saturase Knock-Out Mice are Characterized by Impaired Clearance of Apoptotic Cells and Develop Mild Autoimmunity.

Zsolt Sarang, Tibor Sághy, Zsófia Budai, László Ujlaky-Nagy, Judit Bedekovics, Lívia Beke, Gábor Méhes, Gábor Nagy, Ralph Rühl, Alexander R Moise and 2 more

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2019. 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
0.7field-weighted citation impact, top 30% 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, 13 citations in OpenAlex.

  1. Article
  2. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. 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

12 authors at 3 institutions in 3 countries.

Zsolt SarangDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen H-4012, Hungary.
Tibor SághyDepartment of Dental Biochemistry, Faculty of Dentistry, University of Debrecen, Debrecen H-4012, Hungary.
Zsófia BudaiDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen H-4012, Hungary.
László Ujlaky-NagyDepartment of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen H-4012, Hungary.
Judit BedekovicsDepartment of Pathology, Faculty of Medicine, University of Debrecen, Debrecen H-4012, Hungary.
Lívia BekeDepartment of Pathology, Faculty of Medicine, University of Debrecen, Debrecen H-4012, Hungary.
Gábor MéhesDepartment of Pathology, Faculty of Medicine, University of Debrecen, Debrecen H-4012, Hungary.
Gábor NagyDepartment of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen H-4012, Hungary.
Ralph RühlPaprika Bioanalytics BT, Debrecen H-4002, Hungary.
Alexander R MoiseMedical Sciences Division, Northern Ontario School of Medicine, Sudbury, ON P3E 2C6, Canada.ORCID 0000-0003-2307-6035
Krzysztof PalczewskiGavin Herbert Eye Institute and the Department of Ophthalmology, University of California, Irvine, CA 92697, USA.ORCID 0000-0002-0788-545X
Zsuzsa SzondyDepartment of Dental Biochemistry, Faculty of Dentistry, University of Debrecen, Debrecen H-4012, Hungary.
University of Debrecen · HUNOSM University · CAUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis and the proper clearance of apoptotic cells play a central role in maintaining tissue homeostasis. Previous work in our laboratory has shown that when a high number of cells enters apoptosis in a tissue, the macrophages that engulf them produce retinoids to enhance their own phagocytic capacity by upregulating several phagocytic genes. Our data indicated that these retinoids might be dihydroretinoids, which are products of the retinol saturase (RetSat) pathway. In the present study, the efferocytosis of RetSat-null mice was investigated. We show that among the retinoid-sensitive phagocytic genes, only transglutaminase 2 responded in macrophages and in differentiating monocytes to dihydroretinol. Administration of dihydroretinol did not affect the expression of the tested genes differently between differentiating wild type and RetSat-null monocytes, despite the fact that the expression of RetSat was induced. However, in the absence of RetSat, the expression of numerous differentiation-related genes was altered. Among these, impaired production of MFG-E8, a protein that bridges apoptotic cells to the α

Indexed as

AgingAnimalsApoptosisAutoimmune DiseasesFemaleMacrophagesMiceMice, KnockoutMonocytesOxidoreductases Acting on CH-CH Group DonorsOxidoreductases Acting on CH-CH Group Donorsretinol saturase (all trans retinol 13,14 reductase), mouseautoimmunityefferocytosismacrophageMFG-E8neuropeptide Yretinol saturase

Identifiers

PMID31766264
PMCPMC6920856
OpenAlexW2985463613

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.