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[Research progress on molecular mechanism related to skeletal muscle atrophy].
Sheng Li Xue Bao
December 2024
Department of Orthopaedics, the First Hospital of Lanzhou University, Lanzhou 730000, China.
The maintenance of skeletal muscle quality involves various signal pathways that interact with each other. Under normal physiological conditions, these intersecting signal pathways regulate and coordinate the hypertrophy and atrophy of skeletal muscles, balancing the protein synthesis and degradation of muscle. When the total rate of protein synthesis exceeds that of protein degradation, the muscle gradually becomes enlarged, while when the total rate of protein synthesis is lower than that of protein degradation, the muscle shrinks.
View Article and Find Full Text PDF[Effect of electroacupuncture on denervated skeletal muscle atrophy in rats based on p38 MAPK signaling pathway].
Zhongguo Zhen Jiu
January 2025
College of TCM, Chongqing Medical University, Chongqing Key Laboratory of TCM for Prevention and Treatment of Metabolic Diseases, Chongqing 410007, China.
Objective: To assess the impacts of electroacupuncture (EA) on the gait, oxidative stress, inflammatory reaction, and protein degradation in the rats of denervated skeletal muscle atrophy, and explore the potential mechanism of EA for alleviating denervated skeletal muscle atrophy.
Methods: Forty male SD rats, 8 weeks old, were randomly assigned to a sham-surgery group, a model group, an EA group, and a p38 MAPK inhibitor group, with 10 rats in each group. The right sciatic nerve was transected to establish a rat model of denervated skeletal muscle atrophy in the model group, the EA group and the p38 MAPK inhibitor group.
Edaravone promotes motoneuron survival and functional recovery after brachial plexus root avulsion and reimplantation in rats: Involvement of SIRT1/TFEB pathway.
Int Immunopharmacol
January 2025
Research Center of Basic Integrative Medicine, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, China; Department of Medical Biotechnology, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, China; Dongguan Institute of Guangzhou University of Chinese Medicine, Dongguan, 523808, China. Electronic address:
Background: Brachial plexu root avulsion (BPRA) commonly causes extensive motoneuron death, motor axon degeneration and denervation of biceps, leading to devastating motor dysfunction in the upper limb. Edaravone (Eda) has been proven to exert anti-oxidative and neuroprotective effects on various neurological disorders. Herein, we aimed to investigate the efficacy profile and potential mechanisms of Eda on BPRA in vitro and in vivo models.
View Article and Find Full Text PDFSMN Deficiency Induces an Early Non-Atrophic Myopathy with Alterations in the Contractile and Excitatory Coupling Machinery of Skeletal Myofibers in the SMN∆7 Mouse Model of Spinal Muscular Atrophy.
Int J Mol Sci
November 2024
Department of Basic Medical Sciences, Institute of Biomedical Technologies (ITB), Universidad de La Laguna, 38200 San Cristobal de la Laguna, Spain.
Article Synopsis
- Spinal muscular atrophy (SMA) is caused by a lack of survival motor neuron (SMN) protein, leading to the degeneration of lower motor neurons and muscle atrophy.
- Early research in SMNΔ7 mice showed signs of motor dysfunction and myofiber changes before muscle denervation occurred, highlighting that SMN deficiency has direct effects on muscle cells.
- The study revealed ultrastructural abnormalities in muscle fibers, including disruptions in the myofibrillar structure and altered mitochondrial dynamics, suggesting that muscle changes occur independently of motor neuron loss in SMA.
Respiratory Trajectories and Correlation with Serum Biochemical Indices in Spinal and Bulbar Muscular Atrophy.
Brain Sci
October 2024
Department of Medical, Surgical and Neurological Sciences, University of Siena, 53100 Siena, Italy.
Background/objectives: The primary life-threatening complication in spinal-bulbar muscular atrophy (SBMA) is ventilatory failure. The present study analyzes the longitudinal patterns of respiratory function tests over a follow-up of 11 years.
Methods: We collected data from 9 genetically confirmed SBMA patients.
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