Evidence map›Paper›PMID 37291645›Full record

ArticleBiological research2023

Cholic and deoxycholic acids induce mitochondrial dysfunction, impaired biogenesis and autophagic flux in skeletal muscle cells.

Johanna Abrigo, Hugo Olguín, Franco Tacchi, Josué Orozco-Aguilar, Mayalen Valero-Breton, Jorge Soto, Mauricio Castro-Sepúlveda, Alvaro A Elorza, Felipe Simon, Claudio Cabello-Verrugio

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
6.5field-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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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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

10 authors at 4 institutions in 2 countries.

Johanna Abrigo *Laboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile.
Hugo Olguín *Laboratory of Tissue Repair and Adult Stem Cells, Department of Cellular and Molecular Biology, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago, Chile.
Franco Tacchi *Laboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile.
Josué Orozco-Aguilar *Laboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile.
Mayalen Valero-BretonLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile.
Jorge SotoMillennium Institute on Immunology and Immunotherapy, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile.
Mauricio Castro-SepúlvedaExercise Physiology and Metabolism Laboratory, School of Kinesiology, Faculty of Medicine, Finis Terrae University, Santiago, Chile.
Alvaro A ElorzaMillennium Institute on Immunology and Immunotherapy, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile.
Felipe SimonMillennium Institute on Immunology and Immunotherapy, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile. fsimon@unab.cl.
Claudio Cabello-VerrugioLaboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile. claudio.cabello@unab.cl.ORCID http://orcid.org/0000-0001-7273-2102
Universidad de Santiago de Chile · CLUniversidad Andrés Bello · CLFinis Terrae University · CLPontificia Universidad Católica de Chile · CL

Funding

Agencia Nacional de Investigación y Desarrollo (ANID) - Millennium Science Initiative Program former P09/016-FAgencia Nacional de Investigación y Desarrollo (ANID) - Millennium Science Initiative Program ICN09_016 / ICN 2021_045: Millennium Institute on ImmunologyAgencia Nacional de Investigación y Desarrollo (ANID) - Millennium Science Initiative Program Immunotherapy (ICN09_016 / ICN 2021_045BASAL Grant - CEDENNA from the National Research and Development Agency (ANID), Government of Chile AFB180001Fondo Nacional de Desarrollo Científico y Tecnológico 1180983Fondo Nacional de Desarrollo Científico y Tecnológico 1200944Fondo Nacional de Desarrollo Científico y Tecnológico 1201039Millennium Nucleus of Ion Channel-Associated Diseases (MiNICAD) Chile)Millennium Nucleus of Ion Channel-Associated Diseases (MiNICAD) Iniciativa Científica Milenio (ANID
6 · The paper itself

Abstract

backgroundSkeletal muscle is sensitive to bile acids (BA) because it expresses the TGR5 receptor for BA. Cholic (CA) and deoxycholic (DCA) acids induce a sarcopenia-like phenotype through TGR5-dependent mechanisms. Besides, a mouse model of cholestasis-induced sarcopenia was characterised by increased levels of serum BA and muscle weakness, alterations that are dependent on TGR5 expression. Mitochondrial alterations, such as decreased mitochondrial potential and oxygen consumption rate (OCR), increased mitochondrial reactive oxygen species (mtROS) and unbalanced biogenesis and mitophagy, have not been studied in BA-induced sarcopenia.

methodsWe evaluated the effects of DCA and CA on mitochondrial alterations in C

resultsDCA and CA caused a reduction in mitochondrial mass and decreased mitochondrial biogenesis. Interestingly, DCA and CA increased LC3II/LC3I ratio and decreased autophagic flux concordant with raised mitophagosome-like structures. In addition, DCA and CA decreased mitochondrial potential and reduced protein levels in OXPHOS complexes I and II. The results also demonstrated that DCA and CA decreased basal, ATP-linked, FCCP-induced maximal respiration and spare OCR. DCA and CA also reduced the number of cristae. In addition, DCA and CA increased the mtROS. In mice with cholestasis-induced sarcopenia, TOM20, OXPHOS complexes I, II and III, and OCR were diminished. Interestingly, the OCR and OXPHOS complexes were correlated with muscle strength and bile acid levels.

conclusionOur results showed that DCA and CA decreased mitochondrial mass, possibly by reducing mitochondrial biogenesis, which affects mitochondrial function, thereby altering potential OCR and mtROS generation. Some mitochondrial alterations were also observed in a mouse model of cholestasis-induced sarcopenia characterised by increased levels of BA, such as DCA and CA.

Indexed as

CholestasisSarcopeniaAnimalsDisease Models, AnimalMiceMitochondriaMuscle Fibers, SkeletalMuscle, SkeletalBile acidsBiogenesisMitochondrial dysfunctionMitophagyOxygen consumptionSkeletal muscle

Identifiers

PMID37291645
PMCPMC10249330
OpenAlexW4379967651

What OpenQuestion holds

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Registered trials

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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.