Evidence map›Paper›PMID 31108462›Full record

ArticleRedox biology2019

Cholesterol enrichment in liver mitochondria impairs oxidative phosphorylation and disrupts the assembly of respiratory supercomplexes.

Estel Solsona-Vilarrasa, Raquel Fucho, Sandra Torres, Susana Nuñez, Natalia Nuño-Lámbarri, Carlos Enrich, Carmen García-Ruiz, José C Fernández-Checa

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

77 citing papers in PubMed, 131 citations in OpenAlex.

  1. Review
  2. Sterol biosynthesis, brain development, and disease.The Journal of clinical investigation · 2026
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17 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 2 countries.

Estel Solsona-VilarrasaDepartment of Cell Death and Proliferation, Institute of Biomedical Research of Barcelona (IIBB), CSIC, Barcelona, Spain; Liver Unit, Hospital Clinic I Provincial de Barcelona, Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Centro de Investigación Biomédica en Red (CIBEREHD), Barcelona, Spain; Department of Biomedical Sciences, Medicine Faculty, Universitat de Barcelona (UB), Spain.
Raquel FuchoDepartment of Cell Death and Proliferation, Institute of Biomedical Research of Barcelona (IIBB), CSIC, Barcelona, Spain; Liver Unit, Hospital Clinic I Provincial de Barcelona, Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Centro de Investigación Biomédica en Red (CIBEREHD), Barcelona, Spain.
Sandra TorresDepartment of Cell Death and Proliferation, Institute of Biomedical Research of Barcelona (IIBB), CSIC, Barcelona, Spain; Liver Unit, Hospital Clinic I Provincial de Barcelona, Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Centro de Investigación Biomédica en Red (CIBEREHD), Barcelona, Spain.
Susana NuñezCentro de Investigación Biomédica en Red (CIBEREHD), Barcelona, Spain.
Natalia Nuño-LámbarriDepartment of Cell Death and Proliferation, Institute of Biomedical Research of Barcelona (IIBB), CSIC, Barcelona, Spain; Liver Unit, Hospital Clinic I Provincial de Barcelona, Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Traslational Research Unit, Medica Sur Clinic & Foundation, Mexico City, Mexico.
Carlos EnrichLiver Unit, Hospital Clinic I Provincial de Barcelona, Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Department of Biomedical Sciences, Medicine Faculty, Universitat de Barcelona (UB), Spain.
Carmen García-RuizDepartment of Cell Death and Proliferation, Institute of Biomedical Research of Barcelona (IIBB), CSIC, Barcelona, Spain; Liver Unit, Hospital Clinic I Provincial de Barcelona, Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Centro de Investigación Biomédica en Red (CIBEREHD), Barcelona, Spain; (e)Research Center for ALPD, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States. Electronic address: cgrbam@iibb.csic.es.
José C Fernández-ChecaDepartment of Cell Death and Proliferation, Institute of Biomedical Research of Barcelona (IIBB), CSIC, Barcelona, Spain; Liver Unit, Hospital Clinic I Provincial de Barcelona, Instituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Centro de Investigación Biomédica en Red (CIBEREHD), Barcelona, Spain; (e)Research Center for ALPD, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States. Electronic address: checa229@yahoo.com.
Consorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESCentro de Investigación Biomédica en Red · ESInstitut d'Investigacions Biomèdiques de Barcelona · ES

Funding

The Southernearch Center for ALPD and CirrhosisP50AA011999 · NIAAA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ANNA S. GUKOVSKAYA · 1999 to 2026
$45.8M
NIAAA NIH HHS P50 AA011999
6 · The paper itself

Abstract

Mitochondrial cholesterol accumulation is a hallmark of alcoholic and non-alcoholic fatty liver diseases and impairs the function of specific solute carriers through changes in membrane physical properties. However, its impact on mitochondrial respiration and organization of respiratory supercomplexes has not been determined so far. Here we fed mice a cholesterol-enriched diet (HC) supplemented with sodium cholate to examine the effect of cholesterol in mitochondrial function. HC feeding increased liver cholesterol content, which downregulated Srebp2 and Hmgcr expression, while sodium cholate administration decreased Cyp7a1 and Cyp8b1 mRNA levels, suggesting the downregulation of bile acid synthesis through the classical pathway. HC-fed mice exhibited increased expression of Stard1 and Mln64 and enhanced mitochondrial free cholesterol levels (2-3 fold), leading to decreased membrane fluidity. Mitochondria from HC-fed mice displayed increased cholesterol loading in both outer and inner mitochondrial membranes. Cholesterol loading decreased complex I and complex II-driven state 3 respiration and mitochondrial membrane potential. Decreased respiratory and uncoupling control ratio from complex I was also observed after in situ enrichment of mouse liver mitochondria with cholesterol or enantiomer cholesterol, the mirror image of natural cholesterol. Moreover, in vivo cholesterol loading decreased the level of complex III

Indexed as

Oxidative PhosphorylationAnimalsBile Acids and SaltsCell RespirationCholesterolElectron Transport Chain Complex ProteinsElectron Transport Complex IExtracellular MatrixHomeostasisLipid MetabolismMaleMembrane Potential, MitochondrialMiceMitochondria, LiverMitochondrial MembranesOxidative StressBile Acids and SaltsCholesterolElectron Transport Chain Complex ProteinsElectron Transport Complex IReactive Oxygen SpeciesCholesterolHepatic diseasesLiverMitochondriaOxidative stressRespiration

Identifiers

PMID31108462
PMCPMC6526464
OpenAlexW2944735878

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.