Evidence map›Paper›PMID 40025530›Full record

ArticleJournal of translational medicine2025

Indole-3-propionic acid promotes hepatic stellate cells inactivation.

Mariana Ilha, Ratika Sehgal, Johanna Matilainen, Kirsi Rilla, Dorota Kaminska, Shrey Gandhi, Ville Männistö, Charlotte Ling, Stefano Romeo, Päivi Pajukanta and 5 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
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  9. Article
  10. Review
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

15 authors.

Mariana IlhaInstitute of Public Health and Clinical Nutrition, Department of Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.
Ratika SehgalInstitute of Public Health and Clinical Nutrition, Department of Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.
Johanna MatilainenInstitute of Biomedicine, School of Medicine, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland.
Kirsi RillaInstitute of Biomedicine, School of Medicine, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland.
Dorota KaminskaInstitute of Public Health and Clinical Nutrition, Department of Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.
Shrey GandhiInstitute of Immunology, University of Münster, Münster, Germany.
Ville MännistöDepartments of Medicine, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland.
Charlotte LingEpigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Scania University Hospital, Malmö, Sweden.
Stefano RomeoDepartment of Molecular and Clinical Medicine, University of Gothenburg, Göteborg, Sweden.
Päivi PajukantaDepartment of Human Genetics, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA, USA.
Eija PirinenResearch Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Kirsi A VirtanenTurku PET Centre, University of Turku, Turku, Finland.
Kirsi H PietiläinenObesity Research Unit, Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Maija VaittinenInstitute of Public Health and Clinical Nutrition, Department of Clinical Nutrition, University of Eastern Finland, Kuopio, Finland. maija.vaittinen@uef.fi.ORCID 0000-0002-7423-557X
Jussi PihlajamäkiInstitute of Public Health and Clinical Nutrition, Department of Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.

Funding

Multimodal omics approach to identify health to cardiometabolic disease transitionsR01HL170604 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Paivi Pajukanta · 2023 to 2026
$2.8M
Methods for Genomic Analysis in Heterogeneous TissuesR01HG010505 · NHGRI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HALPERIN, ERAN · 2019 to 2022
$2.6M
Genetics of adipose cell-type expression and cardiometabolic traitsR01DK132775 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MOHLKE, KAREN L., PAJUKANTA, PAIVI · 2022 to 2025
$2.4M
Academy of Finland 138006Academy of Finland 266286Academy of Finland 272376Academy of Finland 314383Academy of Finland 314454Academy of Finland 314455Academy of Finland 314456Academy of Finland 316458Academy of Finland 324494Academy of Finland 335443Academy of Finland 335445Academy of Finland 335446Academy of Finland 336449Academy of Finland 337120Health from Science 404030Horizon 2020 Framework Programme of the European Union 740264Kuopio University Hospital EVO/VTR grants 2005-2019National Institutes of Health (NIH) R01DK132775National Institutes of Health (NIH) R01HG010505National Institutes of Health (NIH) R01HL170604NHGRI NIH HHS R01 HG010505NHLBI NIH HHS R01 HL170604NIDDK NIH HHS R01 DK132775Novo Nordisk Foundation NNF10OC1013354Novo Nordisk Foundation NNF17OC0027232Novo Nordisk Foundation NNF20OC0060547Swedish Foundation for the Strategic Research Dnr IRC15-0067Wellcome Trust 335444
6 · The paper itself

Abstract

BACKGROUND &

aimsWe have previously reported that the serum levels of gut-derived tryptophan metabolite indole-3-propionic acid (IPA) are lower in individuals with liver fibrosis. Now, we explored the transcriptome and DNA methylome associated with serum IPA levels in human liver from obese individuals together with IPA effects on shifting the hepatic stellate cell (HSC) phenotype to inactivation in vitro.

methodsA total of 116 obese individuals without type 2 diabetes (T2D) (age 46.8 ± 9.3 years; BMI: 42.7 ± 5.0 kg/m

resultsSerum IPA levels were associated with the expression of liver genes enriched for apoptosis, mitophagy and longevity pathways in the liver. AKT serine/threonine kinase 1 (AKT1) was the shared and topmost interactive gene from the liver transcript and DNA methylation profile. IPA treatment induced apoptosis, reduced mitochondrial respiration as well as modified cell morphology, and mitochondrial dynamics by modulating the expression of genes known to regulate fibrosis, apoptosis, and survival in LX-2 cells.

conclusionIn conclusion, these data support that IPA has a plausible therapeutic effect and may induce apoptosis and the HSC phenotype towards the inactivation state, extending the possibilities to suppress hepatic fibrogenesis by interfering with HSC activation and mitochondrial metabolism.

Indexed as

Hepatic Stellate CellsIndolesPropionatesApoptosisCell LineDNA MethylationFemaleGene Expression RegulationHumansLiverLiver CirrhosisMaleMiddle AgedMitochondriaObesityTranscriptomeindolepropionic acidIndolesPropionatesApoptosisEpigeneticsHepatic stellate cellsIndole-3-propionic acidLiver fibrosisMitochondrial metabolism

Identifiers

PMID40025530
PMCPMC11871697

What Socratic 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 Socratic graph.