Evidence map›Paper›PMID 39726152›Full record

ArticleThe FEBS journal2025

Inhibition of intracellular versus extracellular cathepsin D differentially alters the liver lipidome of mice with metabolic dysfunction-associated steatohepatitis.

Isabeau Vermeulen, Mengying Li, Hester van Mourik, Tulasi Yadati, Gert Eijkel, Benjamin Balluff, Roger Godschalk, Lieve Temmerman, Erik A L Biessen, Aditya Kulkarni and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The FEBS journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Nutrients · 2025
    Trial
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

14 authors.

Isabeau VermeulenMaastricht Multimodal Molecular Imaging Institute (M4i), University of Maastricht, The Netherlands.
Mengying LiDepartment of Genetics and Cell Biology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, The Netherlands.
Hester van MourikDepartment of Genetics and Cell Biology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, The Netherlands.
Tulasi YadatiDepartment of Genetics and Cell Biology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, The Netherlands.
Gert EijkelMaastricht Multimodal Molecular Imaging Institute (M4i), University of Maastricht, The Netherlands.
Benjamin BalluffMaastricht Multimodal Molecular Imaging Institute (M4i), University of Maastricht, The Netherlands.
Roger GodschalkDepartment of Pharmacology and Toxicology, Institute for Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, The Netherlands.
Lieve TemmermanDepartment of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center (UMC), The Netherlands.
Erik A L BiessenDepartment of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center (UMC), The Netherlands.
Aditya KulkarniAten Porus Lifesciences Pvt Ltd, Bengaluru, India.
Jan TheysDepartment of Precision Medicine, Institute for Oncology and Reproduction (GROW), Maastricht University, The Netherlands.
Tom HoubenDepartment of Genetics and Cell Biology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, The Netherlands.
Berta Cillero-PastorMaastricht Multimodal Molecular Imaging Institute (M4i), University of Maastricht, The Netherlands.
Ronit Shiri-SverdlovDepartment of Genetics and Cell Biology, Institute of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, The Netherlands.ORCID 0000-0002-6736-7814

Funding

Chinese Scholarship CouncilDutch Province of Limburg
6 · The paper itself

Abstract

The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) progressing to metabolic dysfunction-associated steatohepatitis (MASH), characterized by hepatic inflammation, has significantly increased in recent years due to unhealthy dietary practices and sedentary lifestyles. Cathepsin D (CTSD), a lysosomal protease involved in lipid homeostasis, is linked to abnormal lipid metabolism and inflammation in MASH. Although primarily intracellular, CTSD can be secreted extracellularly. Our previous proteomics research has shown that inhibition of extracellular CTSD results in more anti-inflammatory effects and fewer potential side effects compared to intracellular CTSD inhibition. However, the correlation between reduced side effects and alterations in the hepatic lipid composition remains unknown. This study aims to investigate the correlation between intra- and extracellular CTSD inhibition and potential alterations in the hepatic lipid composition in MASH. Low-density lipoprotein receptor knockout (Ldlr

Indexed as

Cathepsin DFatty LiverLipid MetabolismLiverNon-alcoholic Fatty Liver DiseaseAnimalsDiet, High-FatLipidomicsMaleMiceMice, Inbred C57BLMice, KnockoutReceptors, LDLCathepsin DCtsd protein, mouseReceptors, LDLcathepsinlipidomicsMALDIsmall‐compound inhibitorssteatotic liver disease

Identifiers

PMID39726152
PMCPMC11970712

What OpenQuestion holds

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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.