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Objective: To establish a cellular-level mechanical injury model for human skeletal muscle cells and investigate changes in the mechanical effect mechanism after such injuries.
Methods: The FX-5000™ Compression System was used to apply constant static mechanical pressure to human skeletal muscle cells. A factorial design analysis was conducted to discover the optimal injury model by evaluating the correlation between the amount of pressure, the duration of mechanical stimulation, and the number of days of observation. Skeletal muscle cell injury was evaluated by measuring cell metabolism, morphology, and calcium homeostasis.
Results: Mechanical injury was modeled as continuous pressure of 1 MPa for 2 hours with observation for 3 days. The results show that mechanical injury increased creatine kinase, intracellular Ca concentration, and malondialdehyde content, decreased superoxide dismutase, and caused cell swelling and severe cytoplasmic vacuolization (all P < 0.05).
Conclusion: This model of mechanically-injured human skeletal muscle cells provides an experimental model for the clinically common skeletal muscle injury caused by static loading pressure. It may be used to study the mechanism of action of treatment methods for mechanically injured skeletal muscle.
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http://dx.doi.org/10.62347/HCXU6226 | DOI Listing |
J Foot Ankle Res
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Department of Exercise Sciences, Brigham Young University, Provo, Utah, USA.
Introduction: Intrinsic foot muscles and the plantar fascia are crucial for foot health, which diminishes with age and conditions such as chronic plantar fasciitis (PF). Ultrasound (US) is an accessible and cost-effective method for evaluating these structures. This study aims to assess the repeatability, reliability, and validity of plantar fascia thickness and flexor digitorum brevis (FDB) muscle measurements using US compared with MRI in individuals with and without PF.
View Article and Find Full Text PDFFASEB J
September 2025
School of Biodiversity, One Health and Veterinary Medicine, Graham Kerr Building, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
Most animals experience abrupt developmental transitions involving major tissue remodeling, but the links with metabolic changes remain poorly understood. We examined ontogenetic changes in mitochondrial volume, oxidative capacity, oxygen consumption capacity, and anaerobic capacity across four organs (gut, liver, heart, and hindlimb muscle) in Xenopus laevis from metamorphosis to adulthood. These organs differ in the extent of developmental transformation.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
September 2025
Integrative Muscle Biology Laboratory, Division of Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, Tennessee, USA.
Background: Cancer promotes muscle wasting through an imbalance in the tightly regulated protein synthesis and degradation processes. An array of intracellular signalling pathways, including mTORC1 and AMPK, regulate protein synthesis, and these pathways are responsive to the muscle's microenvironment and systemic stimuli. Although feeding and fasting are established systemic regulators of muscle mTORC1 and protein synthesis, the cancer environment's impact on these responses during cachexia development is poorly understood.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
October 2025
Department of Surgery, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, the Netherlands.
Background: Body composition alterations such as skeletal muscle (SM) loss in cancer patients are associated with poor survival. In turn, immune cell-driven pathways have been linked to muscle wasting. We aimed to investigate the relationship between body composition, tumour-infiltrating lymphocytes and survival in patients with advanced lung cancer.
View Article and Find Full Text PDFLab Anim Res
September 2025
Department of Pathology, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka, 589-8511, Japan.
Background: Stroke-prone spontaneously hypertensive rats (SHRSP) exhibit slow-twitch muscle-specific hypotrophy compared with normotensive Wistar-Kyoto rats (WKY). Because slow-twitch muscles are prone to disuse atrophy, SHRSP may experience both disuse atrophy and impaired recovery from it. This study investigated the response of SHRSP to disuse atrophy and subsequent recovery, using WKY as a control.
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