Evidence map›Paper›PMID 36359900›Full record

ArticleCells2022

The HSF1-CPT1a Pathway Is Differentially Regulated in NAFLD Progression.

Wiebke Breternitz, Friedrich Sandkühler, Frauke Grohmann, Jochen Hampe, Mario Brosch, Alexander Herrmann, Clemens Schafmayer, Christian Meinhardt, Stefan Schreiber, Alexander Arlt and 1 more

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

Article in Cells, 2022. 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
0.8field-weighted citation impact, top 28% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. Article
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

11 authors at 4 institutions in 1 country.

Wiebke BreternitzLaboratory of Molecular Gastroenterology & Hepatology, Department of Internal Medicine I, UKSH-Campus Kiel, 24105 Kiel, Germany.
Friedrich SandkühlerLaboratory of Molecular Gastroenterology & Hepatology, Department of Internal Medicine I, UKSH-Campus Kiel, 24105 Kiel, Germany.
Frauke GrohmannLaboratory of Molecular Gastroenterology & Hepatology, Department of Internal Medicine I, UKSH-Campus Kiel, 24105 Kiel, Germany.
Jochen HampeMedical Department 1, University Hospital Dresden, Dresden University of Technology (TU Dresden), 01307 Dresden, Germany.
Mario BroschMedical Department 1, University Hospital Dresden, Dresden University of Technology (TU Dresden), 01307 Dresden, Germany.
Alexander HerrmannMedical Department 1, University Hospital Dresden, Dresden University of Technology (TU Dresden), 01307 Dresden, Germany.
Clemens SchafmayerDepartment of General, Visceral, Vascular and Transplantation Surgery, University of Rostock, 18057 Rostock, Germany.
Christian MeinhardtDepartment for Gastroenterology and Hepatology, University Hospital Oldenburg, Klinikum Oldenburg AöR, European Medical School (EMS), 26133 Oldenburg, Germany.
Stefan SchreiberLaboratory of Molecular Gastroenterology & Hepatology, Department of Internal Medicine I, UKSH-Campus Kiel, 24105 Kiel, Germany.
Alexander ArltDepartment for Gastroenterology and Hepatology, University Hospital Oldenburg, Klinikum Oldenburg AöR, European Medical School (EMS), 26133 Oldenburg, Germany.ORCID 0000-0002-6160-1059
Claudia GeismannLaboratory of Molecular Gastroenterology & Hepatology, Department of Internal Medicine I, UKSH-Campus Kiel, 24105 Kiel, Germany.ORCID 0000-0003-0640-9256
University Hospital Schleswig-Holstein · DETechnische Universität Dresden · DEKlinikum Oldenburg · DEUniversity of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity and obesity-associated diseases represent one of the key health challenges of our time. In this context, aberrant hepatic lipid accumulation is a central pathological aspect of non-alcoholic fatty liver disease (NAFLD). By comparing methylation signatures of liver biopsies before and after bariatric surgery, we recently demonstrated the strong enrichment of differentially methylated heat shock factor 1 (HSF1) binding sites (>400-fold) in the process of liver remodeling, indicating a crucial role of HSF1 in modulating central aspects of NAFLD pathogenesis. Using cellular models of NAFLD, we were able to show that HSF1 is activated during fat accumulation in hepatocytes, mimicking conditions in patients before bariatric surgery. This induction was abolished by starving the cells, mimicking the situation after bariatric surgery. Regarding this connection, carnitine palmitoyltransferase 1 isoform A (CTP1a), a central regulator of lipid beta-oxidation, was identified as a HSF1 target gene by promoter analysis and HSF1 knockdown experiments. Finally, pharmacological activation of HSF1 through celastrol reduced fat accumulation in the cells in a HSF1-dependent manner. In conclusion, we were able to confirm the relevance of HSF1 activity and described a functional HSF1-CPT1a pathway in NAFLD pathogenesis.

Indexed as

Non-alcoholic Fatty Liver DiseaseHumansLipid MetabolismLipidsObesityLipidsbariatric surgeryDNA-methylationlipid oxidationNAFLD

Identifiers

PMID36359900
PMCPMC9655849
OpenAlexW4308446461

What OpenQuestion holds

Textmetadata
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.