Evidence map›Paper›PMID 28970532›Full record

ArticleScientific reports2017

Blood-derived macrophages prone to accumulate lysosomal lipids trigger oxLDL-dependent murine hepatic inflammation.

Tom Houben, Yvonne Oligschlaeger, Albert V Bitorina, Tim Hendrikx, Sofie M A Walenbergh, Marie-Hélène Lenders, Marion J J Gijbels, Fons Verheyen, Dieter Lütjohann, Marten H Hofker and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Lysosomal swelling triggers LRRK2 activity.bioRxiv : the preprint server for biology · 2025
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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 4 institutions in 3 countries.

Tom HoubenDepartments of Molecular Genetics, Molecular Cell Biology and Electron Microscopy, School of Nutrition and Translational Research in Metabolism (NUTRIM), University of Maastricht; Universiteitssingel 50, ER 6229 ER, Maastricht, The Netherlands.ORCID 0000-0002-0441-3166
Yvonne OligschlaegerDepartments of Molecular Genetics, Molecular Cell Biology and Electron Microscopy, School of Nutrition and Translational Research in Metabolism (NUTRIM), University of Maastricht; Universiteitssingel 50, ER 6229 ER, Maastricht, The Netherlands.
Albert V BitorinaDepartments of Molecular Genetics, Molecular Cell Biology and Electron Microscopy, School of Nutrition and Translational Research in Metabolism (NUTRIM), University of Maastricht; Universiteitssingel 50, ER 6229 ER, Maastricht, The Netherlands.
Tim HendrikxDepartments of Molecular Genetics, Molecular Cell Biology and Electron Microscopy, School of Nutrition and Translational Research in Metabolism (NUTRIM), University of Maastricht; Universiteitssingel 50, ER 6229 ER, Maastricht, The Netherlands.
Sofie M A WalenberghDepartments of Molecular Genetics, Molecular Cell Biology and Electron Microscopy, School of Nutrition and Translational Research in Metabolism (NUTRIM), University of Maastricht; Universiteitssingel 50, ER 6229 ER, Maastricht, The Netherlands.
Marie-Hélène LendersDepartments of Molecular Genetics, Molecular Cell Biology and Electron Microscopy, School of Nutrition and Translational Research in Metabolism (NUTRIM), University of Maastricht; Universiteitssingel 50, ER 6229 ER, Maastricht, The Netherlands.
Marion J J GijbelsDepartments of Molecular Genetics, Molecular Cell Biology and Electron Microscopy, School of Nutrition and Translational Research in Metabolism (NUTRIM), University of Maastricht; Universiteitssingel 50, ER 6229 ER, Maastricht, The Netherlands.
Fons VerheyenDepartments of Molecular Genetics, Molecular Cell Biology and Electron Microscopy, School of Nutrition and Translational Research in Metabolism (NUTRIM), University of Maastricht; Universiteitssingel 50, ER 6229 ER, Maastricht, The Netherlands.
Dieter LütjohannInstitute of Clinical Chemistry and Clinical Pharmacology, University of Bonn; Sigmund-Freud-Str. 25, D-53127, Bonn, Germany.
Marten H HofkerDepartment of Pathology and Medical Biology, Molecular Genetics, Medical Biology Section, University of Groningen, University Medical Center Groningen; Hanzeplein 1, 9713 GZ, Groningen, The Netherlands.
Christoph J BinderDepartment of Laboratory Medicine, Medical University of Vienna; Spitalgasse 23, 1090, Vienna, Austria.
Ronit Shiri-SverdlovDepartments of Molecular Genetics, Molecular Cell Biology and Electron Microscopy, School of Nutrition and Translational Research in Metabolism (NUTRIM), University of Maastricht; Universiteitssingel 50, ER 6229 ER, Maastricht, The Netherlands. r.sverdlov@maastrichtuniversity.nl.
Maastricht University · NLKaiser-Franz-Josef-Spital · ATUniversity Medical Center Groningen · NLUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the consistent rise of non-alcoholic steatohepatitis (NASH) worldwide, the mechanisms that govern the inflammatory aspect of this disease remain unknown. Previous research showed an association between hepatic inflammation and lysosomal lipid accumulation in blood-derived hepatic macrophages. Additionally, in vitro findings indicated that lipids, specifically derived from the oxidized low-density lipoprotein (oxLDL) particle, are resistant to removal from lysosomes. On this basis, we investigated whether lysosomal lipid accumulation in blood-derived hepatic macrophages is causally linked to hepatic inflammation and assessed to what extent increasing anti-oxLDL IgM autoantibodies can affect this mechanism. By creating a proof-of-concept mouse model, we demonstrate a causal role for lysosomal lipids in blood-derived hepatic macrophages in mediating hepatic inflammation and initiation of fibrosis. Furthermore, our findings show that increasing anti-oxLDL IgM autoantibody levels reduces inflammation. Hence, therapies aimed at improving lipid-induced lysosomal dysfunction and blocking oxLDL-formation deserve further investigation in the context of NASH.

Indexed as

AnimalsAutoantibodiesCholesterolDisease Models, AnimalHumansImmunoglobulin MInflammationKupffer CellsLipidsLipoproteins, LDLLiverLysosomesMacrophagesMiceNon-alcoholic Fatty Liver DiseaseAutoantibodiesCholesterolImmunoglobulin MLipidsLipoproteins, LDLoxidized low density lipoprotein

Identifiers

PMID28970532
PMCPMC5624963
OpenAlexW2757854240

What OpenQuestion holds

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Registered trials

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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.