Evidence map›Paper›PMID 40879940›Full record

ReviewAdvances in experimental medicine and biology2025

Muscle Disuse Atrophy.

Dongwook Yeo

Abstract readReview
PubMed Publisher
In one paragraph

Review in Advances in experimental medicine and biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

1 author.

Dongwook YeoDepartment of Orthopedic Surgery, Mayo Clinic, Rochester, MN, USA. Yeo.Dongwook@mayo.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscle disuse atrophy is characterized by a significant reduction in skeletal muscle mass and strength, primarily induced by prolonged periods of inactivity and inadequate mechanical stimulus. This condition is frequently encountered in clinical scenarios, especially in cases where patients undergo limb immobilization due to injuries or suffer from spinal cord impairments. The severity of muscle atrophy is often exacerbated by additional factors, such as advancing age and nutritional deficiencies, underscoring the multifaceted nature of this condition. Over the last two decades, significant advancements have been made in understanding the processes that lead to muscle degradation. Insights into the molecular and cellular mechanisms driving muscle catabolism in the absence of regular physical activity have been gained through research utilizing rodent models such as hindlimb unloading and immobilization, denervation, and spinal cord isolation. These experimental models have provided information on the morphological and functional deterioration as well as the extent of understanding of the molecular and cellular processes in response to disuse-induced muscle wasting. Despite these efforts, the therapeutic options for ameliorating muscle disuse atrophy are limited. Resistance training has been identified as the most effective intervention for reversing muscle mass and strength loss, yet it may only be feasible for some patients due to physical limitations or a lack of motivation to engage in intensive exercise routines. In response to these challenges, ongoing research is focused on identifying alternative therapeutic strategies, encompassing both pharmacological and non-pharmacological approaches, aimed at either preventing the onset of muscle atrophy or facilitating recovery following atrophic events. The implications of muscle disuse atrophy extend beyond clinical manifestations, impacting individuals' quality of life by impairing physical endurance and the capacity to perform daily activities. This chapter aims to offer an exhaustive summary of the various signals, pathways, and breakdown mechanisms implicated in muscle atrophy. Additionally, it will present the latest developments in therapeutic strategies addressing this condition.

Indexed as

Muscle, SkeletalMuscular AtrophyMuscular Disorders, AtrophicAnimalsHumansAutophagyMitochondriaMuscle atrophyPgc-1alphaUbiquitin proteasome

Identifiers

What OpenQuestion holds

Textmetadata
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.