Evidence map›Paper›PMID 29057166›Full record

ArticleCurrent pathobiology reports2017

Regulation of Exercise-Induced Autophagy in Skeletal Muscle.

Altea Rocchi, Congcong He

Abstract read
In one paragraph

Article in Current pathobiology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-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

29 citing papers in PubMed, 57 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

2 authors at 1 institution in 1 country.

Altea RocchiDepartment of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Congcong HeDepartment of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Northwestern University · US

Funding

A novel autophagy gene beclin 2 in the prevention of type 2 diabetes and obesityR00DK094980 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HE, CONGCONG · 2014 to 2016
$728k
NIDDK NIH HHS R00 DK094980
6 · The paper itself

Abstract

purpose of reviewPhysical exercise is a highly effective method to prevent several pathogenic conditions, such as obesity, type 2 diabetes and cardiovascular diseases, largely due to metabolic adaptations induced by exercise in skeletal muscle. Yet how exercise induces the beneficial effects in muscle remains to be fully elucidated. Autophagy is a lysosomal degradation pathway that regulates nutrient recycling, energy production and organelle quality control. The autophagy pathway is upregulated in response to stress during exercise and muscle contraction, and may be an important mechanism mediating exercise-induced health benefits. RECENT

findingsA number of studies have indicated that physical exercise induces non-selective autophagy and selective mitophagy in skeletal muscle in animal models and humans. The AMPK-ULK1 and the FoxO3 signaling pathways play an essential role in the activation of the upstream autophagy machinery in skeletal muscle during exercise. The autophagy activity is required for health benefits of exercise, as in different autophagy-deficient mouse lines exercise-induced effects are abolished. SUMMARY: This review aims to summarize and highlight the most recent findings on the role of autophagy in muscle maintenance, the molecular pathways that upregulate autophagy during exercise, and the potential functions of exercise-induced autophagy and mitophagy in skeletal muscle.

Indexed as

AMP-activated protein kinaseAutophagyForkhead box protein transcription factor 3MitophagyPhysical exerciseSkeletal muscle

Identifiers

PMID29057166
PMCPMC5646231
OpenAlexW2605987402

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.