Evidence map›Paper›PMID 30367898›Full record

ArticleJournal of hepatology2019

Impaired endothelial autophagy promotes liver fibrosis by aggravating the oxidative stress response during acute liver injury.

Maria Ruart, Laia Chavarria, Genís Campreciós, Nuria Suárez-Herrera, Carla Montironi, Sergi Guixé-Muntet, Jaume Bosch, Scott L Friedman, Juan Carlos Garcia-Pagán, Virginia Hernández-Gea

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Journal of hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 141 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed, 2 pooled it
13.1field-weighted citation impact, top 1% 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

141 citing papers in PubMed, 2 syntheses or guidelines pooled it, 263 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Protective effects ofRedox report : communications in free radical research · 2026
    Article
  4. Autophagy in MASLD: A Metabolic and Precision Medicine Perspective.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
  5. Article
  6. Article
  7. Association of the Modified Endothelial Activation and Stress Index with MASLD and Liver Fibrosis: Effect Modification by Magnesium Intake.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026
    Article
  8. Review
  9. Article
  10. Autophagy in the liver.Autophagy reports · 2026
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. RasGRP4 Exacerbates Diabetic Kidney Fibrosis via Aloxe3-Mediated Oxidative Stress and Scar-Associated Macrophage Activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  19. Review
  20. Article

81 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 3 countries.

Maria RuartBarcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Spain.
Laia ChavarriaBarcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Spain.
Genís CampreciósBarcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Spain; Centro de Investigación Biomédica Red de enfermedades hepáticas y digestivas, Spain.
Nuria Suárez-HerreraBarcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Spain.
Carla MontironiPathology Department, Liver Cancer Translational Research Laboratory, BCLC Group, IDIBAPS, Liver Unit, Hospital Clinic, Spain.
Sergi Guixé-MuntetSwiss Liver Centre, Inselspital, Bern University, CH, Switzerland.
Jaume BoschBarcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Spain; Centro de Investigación Biomédica Red de enfermedades hepáticas y digestivas, Spain; Swiss Liver Centre, Inselspital, Bern University, CH, Switzerland.
Scott L FriedmanDivision of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, United States.
Juan Carlos Garcia-PagánBarcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Spain; Centro de Investigación Biomédica Red de enfermedades hepáticas y digestivas, Spain.
Virginia Hernández-GeaBarcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Spain; Centro de Investigación Biomédica Red de enfermedades hepáticas y digestivas, Spain. Electronic address: vihernandez@clinic.cat.
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESUniversitat de Barcelona · ESUniversity Hospital of Bern · CHConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESIcahn School of Medicine at Mount Sinai · US

Funding

The Role of KLF6 in Hepatic FibrosisR01DK056621 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI FRIEDMAN, SCOTT L. · 2000 to 2019
$6.2M
NIDDK NIH HHS R01 DK056621
6 · The paper itself

Abstract

BACKGROUND &

aimsEndothelial dysfunction plays an essential role in liver injury, yet the phenotypic regulation of liver sinusoidal endothelial cells (LSECs) remains unknown. Autophagy is an endogenous protective system whose loss could undermine LSEC integrity and phenotype. The aim of our study was to investigate the role of autophagy in the regulation of endothelial dysfunction and the impact of its manipulation during liver injury.

methodsWe analyzed primary isolated LSECs from Atg7

resultsAutophagy maintains LSEC homeostasis and is rapidly upregulated during capillarization in vitro and in vivo. Pharmacological and genetic downregulation of endothelial autophagy increases oxidative stress in vitro. During liver injury in vivo, the selective loss of endothelial autophagy leads to cellular dysfunction and reduced intrahepatic nitric oxide. The loss of autophagy also impairs LSECs ability to handle oxidative stress and aggravates fibrosis.

conclusionsAutophagy contributes to maintaining endothelial phenotype and protecting LSECs from oxidative stress during early phases of liver disease. Selectively potentiating autophagy in LSECs during early stages of liver disease may be an attractive approach to modify the disease course and prevent fibrosis progression. LAY SUMMARY: Liver endothelial cells are the first liver cell type affected after any kind of liver injury. The loss of their unique phenotype during injury amplifies liver damage by orchestrating the response of the liver microenvironment. Autophagy is a mechanism involved in the regulation of this initial response and its manipulation can modify the progression of liver damage.

Indexed as

LiverLiver CirrhosisAnimalsAutophagyBiological AvailabilityDisease ProgressionDown-RegulationEndothelial CellsHepatocytesLiver Failure, AcuteMiceMicrovesselsNitric OxideOxidative StressRatsNitric OxideAtg7AutophagyEndothelial cellEndothelial dysfunctioneNOSLiver fibrosisLSECNitric oxideNrf2Oxidative stress

Identifiers

PMID30367898
PMCPMC6704477
OpenAlexW2898537477

What OpenQuestion holds

Textmetadata
LicenceTDM
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.