Evidence map›Paper›PMID 40127780›Full record

ArticleMolecular metabolism2025

Physical training reduces cell senescence and associated insulin resistance in skeletal muscle.

Agnieszka Podraza-Farhanieh, Rosa Spinelli, Federica Zatterale, Annika Nerstedt, Silvia Gogg, Matthias Blüher, Ulf Smith

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PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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

7 authors.

Agnieszka Podraza-FarhaniehLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, 41345, Sweden.
Rosa SpinelliLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, 41345, Sweden; Department of Translational Medical Sciences, Federico II University of Naples, Naples, 80131, Italy.
Federica ZatteraleLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, 41345, Sweden; Department of Translational Medical Sciences, Federico II University of Naples, Naples, 80131, Italy.
Annika NerstedtLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, 41345, Sweden.
Silvia GoggLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, 41345, Sweden.
Matthias BlüherHelmholtz Institute for Metabolic, Obesity and Vascular Research of the Helmholtz Zentrum München at the University of Leipzig and University Hospital Leipzig, Leipzig, 04103, Germany.
Ulf SmithLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, 41345, Sweden. Electronic address: ulf.smith@medic.gu.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCell senescence (CS) is a key aging process that leads to irreversible cell cycle arrest and an altered secretory phenotype. In skeletal muscle (SkM), the accumulation of senescent cells contributes to sarcopenia. Despite exercise being a known intervention for maintaining SkM function and metabolic health, its effects on CS remain poorly understood.

objectivesThis study aimed to investigate the impact of exercise on CS in human SkM by analyzing muscle biopsies from young, normal-weight individuals and middle-aged individuals with obesity, both before and after exercise intervention.

methodsMuscle biopsies were collected from both groups before and after an exercise intervention. CS markers, insulin sensitivity (measured with euglycemic clamp), and satellite cell markers were analyzed. Additionally, in vitro experiments were conducted to evaluate the effects of cellular senescence on human satellite cells, focusing on key regulatory genes and insulin signaling.

resultsIndividuals with obesity showed significantly elevated CS markers, along with reduced expression of GLUT4 and PAX7, indicating impaired insulin action and regenerative potential. Exercise improved insulin sensitivity, reduced CS markers, and activated satellite cell response in both groups. In vitro experiments revealed that senescence downregulated key regulatory genes in satellite cells and impaired insulin signaling by reducing the Insulin Receptor β-subunit.

conclusionsThese findings highlight the role of CS in regulating insulin sensitivity in SkM and underscore the therapeutic potential of exercise in mitigating age- and obesity-related muscle dysfunction. Targeting CS through exercise or senolytic agents could offer a promising strategy for improving metabolic health and combating sarcopenia, particularly in at-risk populations.

Indexed as

Cellular SenescenceExerciseInsulin ResistanceMuscle, SkeletalAdultFemaleGlucose Transporter Type 4HumansInsulinMaleMiddle AgedObesityPAX7 Transcription FactorSatellite Cells, Skeletal MuscleYoung AdultGlucose Transporter Type 4InsulinPAX7 protein, humanPAX7 Transcription FactorSLC2A4 protein, humanAgingCellular senescenceExercise interventionObesitySatellite cellsSkeletal muscles

Identifiers

PMID40127780
PMCPMC11994356

What Socratic 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 Socratic graph.