Disuse atrophy of human skeletal muscle: cell signaling and potential interventions
- PMID: 19727028
- DOI: 10.1249/MSS.0b013e3181a6458a
Disuse atrophy of human skeletal muscle: cell signaling and potential interventions
Abstract
In response to atrophic stimuli, physical alterations include decreases in fiber diameter and contractile protein content. Despite the fact that these phenotypical alterations have been well characterized, the signaling pathways that mediate these adaptations are still under investigation. There have been significant advances in the past few years delineating signal transduction pathways that regulate protein turnover. In the process of evaluating the effect of various atrophy-inducing stimuli on signal transduction pathways in skeletal muscle, it is apparent that differences do exist concerning both transcriptional and translational adaptations. To this end, it is hypothesized that the processes responsible for invoking skeletal muscle atrophy are unique, despite similar upstream signals and downstream phenotypical adaptations. If this is the case, countermeasures to attenuate atrophy may be more effective if they are designed to accommodate molecular alterations specific to the atrophic stimulus. The aim of this review was to characterize the recent work in humans elucidating the molecular basis of skeletal muscle atrophy in response to immobilization, unloading, spinal cord injury, and detraining to highlight the possibility that all skeletal muscle atrophy is not the same. With an increased understanding of the unique signaling pathways that regulate skeletal muscle protein turnover in the face of various atrophy models, it is possible to exploit these pathways to develop countermeasures to prevent or attenuate atrophy. Eugenics, gene therapy, pharmacology, nutritional, and physical countermeasures are discussed concerning their potential to treat or mitigate atrophy.
Similar articles
-
Regulation of muscle atrophy: wasting away from the outside in: an introduction.Med Sci Sports Exerc. 2009 Oct;41(10):1856-9. doi: 10.1249/MSS.0b013e3181a643b2. Med Sci Sports Exerc. 2009. PMID: 19727029
-
In vivo alterations in skeletal muscle form and function after disuse atrophy.Med Sci Sports Exerc. 2009 Oct;41(10):1869-75. doi: 10.1249/MSS.0b013e3181a645a6. Med Sci Sports Exerc. 2009. PMID: 19727027 Review.
-
Signaling mechanisms involved in disuse muscle atrophy.Med Hypotheses. 2007;69(2):310-21. doi: 10.1016/j.mehy.2006.11.043. Epub 2007 Mar 21. Med Hypotheses. 2007. PMID: 17376604 Review.
-
Muscle apoptotic response to denervation, disuse, and aging.Med Sci Sports Exerc. 2009 Oct;41(10):1876-86. doi: 10.1249/MSS.0b013e3181a6470b. Med Sci Sports Exerc. 2009. PMID: 19727026 Review.
-
Newton's force as countermeasure for disuse atrophy.J Appl Physiol (1985). 2009 Jul;107(1):6-7. doi: 10.1152/japplphysiol.00499.2009. Epub 2009 May 14. J Appl Physiol (1985). 2009. PMID: 19443745 No abstract available.
Cited by
-
5'-UMP inhibited muscle atrophy due to detraining: a randomized, double-blinded, placebo-controlled, parallel-group comparative study.Front Sports Act Living. 2024 Jul 15;6:1403215. doi: 10.3389/fspor.2024.1403215. eCollection 2024. Front Sports Act Living. 2024. PMID: 39076851 Free PMC article.
-
Deciphering the Therapeutic Role of Lactate in Combating Disuse-Induced Muscle Atrophy: An NMR-Based Metabolomic Study in Mice.Molecules. 2024 May 9;29(10):2216. doi: 10.3390/molecules29102216. Molecules. 2024. PMID: 38792078 Free PMC article.
-
Mechanism of skeletal muscle atrophy after spinal cord injury: A narrative review.Front Nutr. 2023 Mar 3;10:1099143. doi: 10.3389/fnut.2023.1099143. eCollection 2023. Front Nutr. 2023. PMID: 36937344 Free PMC article. Review.
-
Single-leg disuse decreases skeletal muscle strength, size, and power in uninjured adults: A systematic review and meta-analysis.J Cachexia Sarcopenia Muscle. 2023 Apr;14(2):684-696. doi: 10.1002/jcsm.13201. Epub 2023 Mar 7. J Cachexia Sarcopenia Muscle. 2023. PMID: 36883219 Free PMC article. Review.
-
Secreted Protein Acidic and Rich in Cysteine as an Exercise-Induced Gene: Towards Novel Molecular Therapies for Immobilization-Related Muscle Atrophy in Elderly Patients.Genes (Basel). 2022 Jun 4;13(6):1014. doi: 10.3390/genes13061014. Genes (Basel). 2022. PMID: 35741776 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Miscellaneous