Evidence map›Paper›PMID 30442920›Full record

ArticleScientific reports2018

Liver-specific Repin1 deficiency impairs transient hepatic steatosis in liver regeneration.

Kerstin Abshagen, Bastian Degenhardt, Marie Liebig, Anna Wendt, Berit Genz, Ute Schaeper, Michael Stumvoll, Ute Hofmann, Marcus Frank, Brigitte Vollmar and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. 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
0.9field-weighted citation impact, top 24% 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, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Therapeutic strategies to improve liver regeneration after hepatectomy.Experimental biology and medicine (Maywood, N.J.) · 2023
    Review
  5. Key hepatoprotective roles of mitochondria in liver regeneration.American journal of physiology. Gastrointestinal and liver physiology · 2023
    Review
  6. Article
  7. Article
  8. 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

11 authors at 6 institutions in 2 countries.

Kerstin AbshagenInstitute for Experimental Surgery, University Medicine Rostock, Schillingallee 69a, 18057, Rostock, Germany. kerstin.abshagen@uni-rostock.de.
Bastian DegenhardtInstitute for Experimental Surgery, University Medicine Rostock, Schillingallee 69a, 18057, Rostock, Germany.
Marie LiebigInstitute for Experimental Surgery, University Medicine Rostock, Schillingallee 69a, 18057, Rostock, Germany.
Anna WendtInstitute for Experimental Surgery, University Medicine Rostock, Schillingallee 69a, 18057, Rostock, Germany.
Berit GenzInstitute for Experimental Surgery, University Medicine Rostock, Schillingallee 69a, 18057, Rostock, Germany.
Ute SchaeperSilence Therapeutics GmbH, Berlin, Robert Rössle Strasse 10, 13125, Berlin, Germany.
Michael StumvollDepartment of Medicine, University of Leipzig, Liebigstrasse 18, 04103, Leipzig, Germany.
Ute HofmannDr. Margarete Fischer-Bosch Institute of Clinical Pharmacology, Auerbachstrasse 112, 70376 Stuttgart and University of Tuebingen, Tuebingen, Germany.
Marcus FrankMedical Biology and Electron Microscopy Centre, University Medicine Rostock, Strempelstrasse 14, 18057, Rostock, Germany.ORCID http://orcid.org/0000-0002-2517-4440
Brigitte VollmarInstitute for Experimental Surgery, University Medicine Rostock, Schillingallee 69a, 18057, Rostock, Germany.
Nora KlötingIntegrated Research and Treatment Center (IFB) Adiposity Diseases, University of Leipzig, Liebigstrasse 19-21, 04103, Leipzig, Germany.
University of Rostock · DEDr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology · DEIFB Adiposity Diseases · DELeipzig University · DEQIMR Berghofer Medical Research Institute · AUSilence Therapeutics (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transient hepatic steatosis upon liver resection supposes functional relationships between lipid metabolism and liver regeneration. Repin1 has been suggested as candidate gene for obesity and dyslipidemia by regulating key genes of lipid metabolism and lipid storage. Herein, we characterized the regenerative potential of mice with a hepatic deletion of Repin1 (LRep1-/-) after partial hepatectomy (PH) in order to determine the functional significance of Repin1 in liver regeneration. Lipid dynamics and the regenerative response were analyzed at various time points after PH. Hepatic Repin1 deficiency causes a significantly decreased transient hepatic lipid accumulation. Defects in lipid uptake, as analyzed by decreased expression of the fatty acid transporter Cd36 and Fatp5, may contribute to attenuated and shifted lipid accumulation, accompanied by altered extent and chronological sequence of liver cell proliferation in LRep1-/- mice. In vitro steatosis experiments with primary hepatocytes also revealed attenuated lipid accumulation and occurrence of smaller lipid droplets in Repin1-deficient cells, while no direct effect on proliferation in HepG2 cells was observed. Based on these results, we propose that hepatocellular Repin1 might be of functional significance for early accumulation of lipids in hepatocytes after PH, facilitating efficient progression of liver regeneration.

Indexed as

Liver RegenerationOrgan SpecificityAnimalsCell ProliferationDNA-Binding ProteinsFatty AcidsFatty LiverGlycogenHepatocytesHep G2 CellsHumansLipid MetabolismLiverLiver Function TestsMaleMice, Inbred C57BLDNA-Binding ProteinsFatty AcidsGlycogenRepin1 protein, mouseRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID30442920
PMCPMC6237840
OpenAlexW2899656402

What OpenQuestion holds

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LicenceCC BY
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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.