Evidence map›Paper›PMID 35219894›Full record

ArticleCellular and molecular gastroenterology and hepatology2022

Autophagy-Related Activation of Hepatic Stellate Cells Reduces Cellular miR-29a by Promoting Its Vesicular Secretion.

Xiaojie Yu, Natalia Elfimova, Marion Müller, Daniel Bachurski, Ulrike Koitzsch, Uta Drebber, Esther Mahabir, Hinrich P Hansen, Scott L Friedman, Sabine Klein and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Autophagy in the liver.Autophagy reports · 2026
    Review
  3. Review
  4. Review
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  6. Article
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  12. Article
  13. Article
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  16. Role of noncoding RNAs in liver fibrosis.World journal of gastroenterology · 2023
    Review
  17. Review
  18. Article
  19. 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

17 authors at 6 institutions in 4 countries.

Xiaojie YuInstitute for Pathology, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Natalia ElfimovaInstitute for Pathology, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany.
Marion MüllerInstitute for Pathology, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Daniel BachurskiDepartment I of Internal Medicine, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany.
Ulrike KoitzschInstitute for Pathology, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Uta DrebberInstitute for Pathology, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany; Center of Integrative Oncology, University Clinic of Cologne and Bonn, Germany.
Esther MahabirCenter for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Hinrich P HansenDepartment I of Internal Medicine, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany; Center of Integrative Oncology, University Clinic of Cologne and Bonn, Germany.
Scott L FriedmanDivision of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Sabine KleinDepartment of Internal Medicine I, University Hospital Frankfurt, Frankfurt, Germany.
Hans Peter DienesInstitute for Pathology, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany.
Marianna HöselInstitute for Pathology, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Reinhard BuettnerInstitute for Pathology, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Center of Integrative Oncology, University Clinic of Cologne and Bonn, Germany.
Jonel TrebickaDepartment of Internal Medicine I, University Hospital Frankfurt, Frankfurt, Germany; European Foundation for the Study of Chronic Liver Failure - EF CLIF, Barcelona, Spain.
Vangelis KondylisInstitute for Pathology, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Inge MannaertsLiver Cell Biology Research Group, Vrije Universiteit Brussel, Brussel, Belgium. Electronic address: inge.mannaerts@vub.be.
Margarete OdenthalInstitute for Pathology, Medical Faculty and University Hospital of Cologne, University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany; Center of Integrative Oncology, University Clinic of Cologne and Bonn, Germany. Electronic address: m.odenthal@uni-koeln.de.
University of Cologne · DEUniversity Hospital Cologne · DEGoethe University Frankfurt · DEIcahn School of Medicine at Mount Sinai · USUniversity Hospital Frankfurt · DEVrije Universiteit Brussel · BE

Funding

Hepatic stellate cells in NASH fibrosis and HCCR01DK128289 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SCOTT L. FRIEDMAN · 2021 to 2026
$2.6M
NIDDK NIH HHS R01 DK128289
6 · The paper itself

Abstract

BACKGROUND &

aimsLiver fibrosis arises from long-term chronic liver injury, accompanied by an accelerated wound healing response with interstitial accumulation of extracellular matrix (ECM). Activated hepatic stellate cells (HSC) are the main source for ECM production. MicroRNA29a (miR-29a) is a crucial antifibrotic miRNA that is repressed during fibrosis, resulting in up-regulation of collagen synthesis.

methodsIntracellular and extracellular miRNA levels of primary and immortalized myofibroblastic HSC in response to profibrogenic stimulation by transforming growth factor β (TGFβ) or platelet-derived growth factor-BB (PDGF-BB) or upon inhibition of vesicular transport and autophagy processes were determined by quantitative polymerase chain reaction. Autophagy flux was studied by electron microscopy, flow cytometry, immunoblotting, and immunocytochemistry. Hepatic and serum miR-29a levels were quantified by using both liver tissue and serum samples from a cohort of chronic hepatitis C virus patients and a murine CCl

resultsIn our study, we show that TGFβ and PDGF-BB resulted in decrease of intracellular miR-29a and a pronounced increase of vesicular miR-29a release into the supernatant. Strikingly, miR-29a vesicular release was accompanied by enhanced autophagic activity and up-regulation of the autophagy marker protein LC3. Moreover, autophagy inhibition strongly prevented miR-29a secretion and repressed its targets' expression such as Col1A1. Consistently, hepatic miR-29a loss and increased LC3 expression in myofibroblastic HSC were associated with increased serum miR-29a levels in CCl

conclusionsWe provide evidence that activation-associated autophagy in HSC induces release of miR-29a, whereas inhibition of autophagy represses fibrogenic gene expression in part through attenuated miR-29a secretion.

Indexed as

Hepatitis C, ChronicAnimalsAutophagyBecaplerminHepatic Stellate CellsHumansLiver CirrhosisMiceMicroRNAsTransforming Growth Factor betaBecaplerminMicroRNAsMIRN29a microRNA, humanMIRN29 microRNA, mouseTransforming Growth Factor betaCirculating MiRNALiver FibrosisMiR-29

Identifiers

PMID35219894
PMCPMC9046234
OpenAlexW4213415654

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.