Evidence map›Paper›PMID 34681883›Full record

ArticleInternational journal of molecular sciences2021

Histone Deacetylase Inhibition Regulates Lipid Homeostasis in a Mouse Model of Amyotrophic Lateral Sclerosis.

Thibaut Burg, Elisabeth Rossaert, Matthieu Moisse, Philip Van Damme, Ludo Van Den Bosch

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 49 citations in OpenAlex.

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  6. Altered Lipid Homeostasis in Mutant FUSMolecular neurobiology · 2025
    Article
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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

5 authors at 1 institution in 1 country.

Thibaut BurgDepartment of Neurosciences, Experimental Neurology, Leuven Brain Institute, KU Leuven-University of Leuven, 3000 Leuven, Belgium.ORCID 0000-0002-8788-2936
Elisabeth RossaertDepartment of Neurosciences, Experimental Neurology, Leuven Brain Institute, KU Leuven-University of Leuven, 3000 Leuven, Belgium.
Matthieu MoisseDepartment of Neurosciences, Experimental Neurology, Leuven Brain Institute, KU Leuven-University of Leuven, 3000 Leuven, Belgium.
Philip Van DammeDepartment of Neurosciences, Experimental Neurology, Leuven Brain Institute, KU Leuven-University of Leuven, 3000 Leuven, Belgium.ORCID 0000-0002-4010-2357
Ludo Van Den BoschDepartment of Neurosciences, Experimental Neurology, Leuven Brain Institute, KU Leuven-University of Leuven, 3000 Leuven, Belgium.ORCID 0000-0003-0104-4067
VIB-KU Leuven Center for Brain & Disease Research · BE

Funding

Fondation Thierry Latran 00099187Muscular Dystrophy Association 577668
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is an incurable and fatal neurodegenerative disorder of the motor system. While the etiology is still incompletely understood, defects in metabolism act as a major contributor to the disease progression. Recently, histone deacetylase (HDAC) inhibition using ACY-738 has been shown to restore metabolic alterations in the spinal cord of a FUS mouse model of ALS, which was accompanied by a beneficial effect on the motor phenotype and survival. In this study, we investigated the specific effects of HDAC inhibition on lipid metabolism using untargeted lipidomic analysis combined with transcriptomic analysis in the spinal cord of FUS mice. We discovered that symptomatic FUS mice recapitulate lipid alterations found in ALS patients and in the SOD1 mouse model. Glycerophospholipids, sphingolipids, and cholesterol esters were most affected. Strikingly, HDAC inhibition mitigated lipid homeostasis defects by selectively targeting glycerophospholipid metabolism and reducing cholesteryl esters accumulation. Therefore, our data suggest that HDAC inhibition is a potential new therapeutic strategy to modulate lipid metabolism defects in ALS and potentially other neurodegenerative diseases.

Indexed as

Disease Models, AnimalAmyotrophic Lateral SclerosisAnimalsFemaleHistone Deacetylase InhibitorsHydroxamic AcidsLipidomicsLipidsMaleMicePyrimidinesRNA-Binding Protein FUSTranscriptomeFUS protein, mouseHistone Deacetylase InhibitorsHydroxamic AcidsLipidsN-hydroxy-2-(1-phenylcycloproylamino)pyrimidine-5-carboxamidePyrimidinesRNA-Binding Protein FUSamyotrophic lateral sclerosisepigeneticFUSglycerophospholipidsHDAC inhibitorshistone deacetylaselipidomicmetabolism

Identifiers

PMID34681883
PMCPMC8541517
OpenAlexW3207668409

What OpenQuestion holds

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LicenceCC BY
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.