Evidence map›Paper›PMID 31195688›Full record

ReviewCells2019

Recent Data on Cellular Component Turnover: Focus on Adaptations to Physical Exercise.

Anthony Mj Sanchez, Robin Candau, Henri Bernardi

Abstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

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  3. Dysregulation of autophagosome-mitochondria contacts contributes to autophagy dysfunction and neurodegeneration in tauopathy.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

3 authors.

Anthony Mj SanchezLaboratoire Européen Performance Santé Altitude, EA4604, University of Perpignan Via Domitia, Faculty of Sports Sciences, F-66120 Font-Romeu, France. anthony.sanchez@univ-perp.fr.ORCID 0000-0003-3054-6349
Robin CandauUniversité de Montpellier, INRA, UMR866 Dynamique Musculaire et Métabolisme, F-34060 Montpellier, France. robin.candau@umontpellier.fr.
Henri BernardiINRA, UMR866 Dynamique Musculaire et Métabolisme, F-34060 Montpellier, France. henri.bernardi@inra.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Significant progress has expanded our knowledge of the signaling pathways coordinating muscle protein turnover during various conditions including exercise. In this manuscript, the multiple mechanisms that govern the turnover of cellular components are reviewed, and their overall roles in adaptations to exercise training are discussed. Recent studies have highlighted the central role of the energy sensor (AMP)-activated protein kinase (AMPK), forkhead box class O subfamily protein (FOXO) transcription factors and the kinase mechanistic (or mammalian) target of rapamycin complex (MTOR) in the regulation of autophagy for organelle maintenance during exercise. A new cellular trafficking involving the lysosome was also revealed for full activation of MTOR and protein synthesis during recovery. Other emerging candidates have been found to be relevant in organelle turnover, especially Parkin and the mitochondrial E3 ubiquitin protein ligase (Mul1) pathways for mitochondrial turnover, and the glycerolipids diacylglycerol (DAG) for protein translation and FOXO regulation. Recent experiments with autophagy and mitophagy flux assessment have also provided important insights concerning mitochondrial turnover during ageing and chronic exercise. However, data in humans are often controversial and further investigations are needed to clarify the involvement of autophagy in exercise performed with additional stresses, such as hypoxia, and to understand the influence of exercise modality. Improving our knowledge of these pathways should help develop therapeutic ways to counteract muscle disorders in pathological conditions.

Indexed as

ExerciseMitochondrial TurnoverAMP-Activated Protein KinasesAutophagyForkhead Transcription FactorsHumansMitophagyMuscle, SkeletalSignal TransductionTOR Serine-Threonine KinasesAMP-Activated Protein KinasesForkhead Transcription FactorsTOR Serine-Threonine KinasesAMPKautophagyexerciseFOXOmitochondriamitophagyMTORparkin

Identifiers

PMID31195688
PMCPMC6627613

What OpenQuestion holds

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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.