Evidence map›Paper›PMID 26351365›Full record

ArticleJournal of lipid research2015

Deoxycholic acid modulates cell death signaling through changes in mitochondrial membrane properties.

Tânia Sousa, Rui E Castro, Sandra N Pinto, Ana Coutinho, Susana D Lucas, Rui Moreira, Cecília M P Rodrigues, Manuel Prieto, Fábio Fernandes

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

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  15. Talk to Me-Interplay between Mitochondria and Microbiota in Aging.International journal of molecular sciences · 2023
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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

9 authors at 1 institution in 1 country.

Tânia SousaCentro de Química-Física Molecular and Institute of Nanoscience and Nanotechnology, Instituto Superior Técnico, University of Lisbon, Lisbon, Portugal.
Rui E CastroResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, University of Lisbon, Lisbon, Portugal.
Sandra N PintoCentro de Química-Física Molecular and Institute of Nanoscience and Nanotechnology, Instituto Superior Técnico, University of Lisbon, Lisbon, Portugal.
Ana CoutinhoCentro de Química-Física Molecular and Institute of Nanoscience and Nanotechnology, Instituto Superior Técnico, University of Lisbon, Lisbon, Portugal Departamento de Química e Bioquímica, Faculty of Sciences, University of Lisbon, Lisbon, Portugal.
Susana D LucasResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, University of Lisbon, Lisbon, Portugal.
Rui MoreiraResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, University of Lisbon, Lisbon, Portugal.
Cecília M P RodriguesResearch Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, University of Lisbon, Lisbon, Portugal.
Manuel PrietoCentro de Química-Física Molecular and Institute of Nanoscience and Nanotechnology, Instituto Superior Técnico, University of Lisbon, Lisbon, Portugal.
Fábio FernandesCentro de Química-Física Molecular and Institute of Nanoscience and Nanotechnology, Instituto Superior Técnico, University of Lisbon, Lisbon, Portugal.
University of Lisbon · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytotoxic bile acids, such as deoxycholic acid (DCA), are responsible for hepatocyte cell death during intrahepatic cholestasis. The mechanisms responsible for this effect are unclear, and recent studies conflict, pointing to either a modulation of plasma membrane structure or mitochondrial-mediated toxicity through perturbation of mitochondrial outer membrane (MOM) properties. We conducted a comprehensive comparative study of the impact of cytotoxic and cytoprotective bile acids on the membrane structure of different cellular compartments. We show that DCA increases the plasma membrane fluidity of hepatocytes to a minor extent, and that this effect is not correlated with the incidence of apoptosis. Additionally, plasma membrane fluidity recovers to normal values over time suggesting the presence of cellular compensatory mechanisms for this perturbation. Colocalization experiments in living cells confirmed the presence of bile acids within mitochondrial membranes. Experiments with active isolated mitochondria revealed that physiologically active concentrations of DCA change MOM order in a concentration- and time-dependent manner, and that these changes preceded the mitochondrial permeability transition. Importantly, these effects are not observed on liposomes mimicking MOM lipid composition, suggesting that DCA apoptotic activity depends on features of mitochondrial membranes that are absent in protein-free mimetic liposomes, such as the double-membrane structure, lipid asymmetry, or mitochondrial protein environment. In contrast, the mechanism of action of cytoprotective bile acids is likely not associated with changes in cellular membrane structure.

Indexed as

ApoptosisAnimalsCells, CulturedCell SurvivalDeoxycholic AcidHepatocytesMaleMembrane FluidityMitochondria, LiverMitochondrial MembranesPermeabilityRatsSignal TransductionDeoxycholic Acidapoptosisbile acids and saltsbile acids and salts/physical chemistryfluorescence microscopymembranesmembranes/fluiditymitochondria

Identifiers

PMID26351365
PMCPMC4617403
OpenAlexW2180308185

What OpenQuestion holds

Textmetadata
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.