Endothelial cystathionine-γ-lyase (CTH) regulates body weight and insulin resistance in mice fed a high-fat diet.

Skeletal muscle in spinal muscular atrophy: Critical insights from pathogenesis to therapeutic strategies.

Temporal Progression of Microvascular Alterations in the Nailfold and Skeletal Muscle of Non-Obese Type 2 Diabetic Rats.

Regulation of skeletal muscle development and metabolism in broiler chickens by Urolithin A through threonine kinase 1 pathway activation.

The role of neprilysin in musculoskeletal diseases.

Analysis of WNT5A as a key regulator of intramuscular fat deposition in muscle-adipocyte co-cultures.

IGF-1 regulates PEAR1 through Egr1 to promote skeletal muscle post-injury regeneration.

Skeletal muscle is a vital part of human physiology and is responsible for numerous essential functions. Not surprisingly, the loss of skeletal muscle mass and function is common in several pathologies including atrophy and sarcopenia, which profoundly impact quality of life of those afflicted. Thus, numerous investigations of potential therapies for mitigating or reversing such pathologies are available. Within these studies, experimental cell culture models such as the murine C2C12 myoblasts are commonly used. Over 100 publications have utilized dexamethasone-treated C2C12 myotubes to investigate various aspects of muscle atrophy. The purpose of this systematic review is to describe the experimental conditions common to these experiments, as well as phenotypical myotube presentation, and gene and protein expression of targets that regulate muscle mass, function, and metabolism. A systematic review of literature was conducted until 3 January 2025 using PUBMED. Articles were included if (1) C2C12 myotubes were used, (2) the article included a dexamethasone-only group along with appropriate vehicle or true control and (3) the article assessed at least one of the related phenotypical or molecular outcomes of importance to the scope of the review. A total of 182 articles were included after screening for relevance and inclusion criteria, which were assessed for outcomes (raw data reported when available or using ratio-metric estimates of relative differences between dexamethasone treatment and control). In 24 of 26 unique experiments that utilized 10 μM dexamethasone and 37 of 39 unique experiments that utilized 100 μM dexamethasone, a decrease in myotube diameter was reported (pooled experimental average estimates from 24-h time points 69.8% ± 7.5% and 66.9% ± 14.7% for 10 and 100 μM, respectively, vs. control). All six studies that utilized 10 μM dexamethasone and all nine that treated myotubes with 100 μM dexamethasone reported reduced fusion index (pooled experimental average estimates from 24-h time points: 67.6% ± 5.3% and 68.4% ± 8.4% for 10 and 100 μM, respectively, vs. control). Dexamethasone-treated myotubes also consistently expressed increased atrophic-related molecular targets including Atrogin-1 and muscle atrophy X box1 (MuRF1), as well as reductions in anabolic signalling (specifically, mTORC and Akt activation) and mitochondrial function. The striking consistency of these findings suggests dexamethasone treatment of C2C12 myotubes is a reliable method of mimicking many features common to skeletal muscle pathology. This review provides insight into the use and expected outcomes of the dexamethasone-mediated model of atrophy in C2C12 myotubes and may serve as a helpful reference for future experiments utilizing this model.

Muscle-specific expression of Atg2 and high-fat diet influence age-related deterioration of skeletal muscle in aged drosophila via the ATGL/Sirt1/PGC-1α pathway.

The effects of acute skeletal muscle wasting on frailty and metabolic profile in patients with trauma: A prospective cohort study.

Usefulness of the bioimpedance phase angle in identifying older adults with poor muscle properties: The Shizuoka study.

Anabolic androgenic steroids are synthetic derivatives of testosterone that mimic its actions in various tissues. Due to its strong anabolic activity, weak androgenic effects, and resistance to hepatic metabolism, oxandrolone is one of the most commonly used anabolic steroids among female athletes. This study aimed to evaluate the anabolic effects of oxandrolone and its toxicological profile in female rats subjected to a strength training protocol. A total of 24 female Wistar rats (60 days old) were randomly assigned to receive oxandrolone (1.77 mg/kg/day) or its vehicle (corn oil) (n = 12 per group) via daily gavage for 28 days. The exercise protocol consisted of six climbs on an inclined ladder, with two climbs per workload (50 %, 75 %, and 100 % of each animal's maximum load) performed three times per week. Investigators remained blinded throughout experimentation and data analysis. Oxandrolone did not significantly affect body weight gain, relative organ and muscle mass, or muscle strength. However, it altered mean corpuscular volume, eosinophil count, and urea levels. Additionally, liver TBARS levels increased, while no changes were observed in plasma lipid peroxidation, antioxidant enzyme activity, total non-protein thiol levels, or mitochondrial respiratory chain complex activity. Histopathological analysis revealed oxandrolone-induced damage to cardiac and skeletal muscle, along with structural alterations in the spleen and adrenal gland. Given its limited effect on muscle strength, along with histopathological changes and increased liver lipoperoxidation, these findings raise concerns about oxandrolone use in healthy individuals seeking aesthetic or athletic benefits.

Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide, and excess adiposity is a major contributor to cardiovascular (CV) risk. However, obesity is a heterogeneous condition, and body mass index (BMI) alone fails to capture important differences in fat distribution and lean mass that substantially influence CV outcomes. Growing clinical and epidemiological evidence indicates that body composition, rather than body weight per se, provides a more accurate and biologically meaningful framework for CV risk assessment. This narrative review summarizes clinical evidence linking key components of body composition, including total and regional adiposity, skeletal muscle mass, and ectopic fat depots, to CV risk and prognosis. Central and visceral adiposity are consistently shown to be more strongly associated with cardiometabolic dysfunction, atherosclerosis, and CV events than generalized obesity. In parallel, reduced lean mass and sarcopenia emerge as independent predictors of adverse CV outcomes, particularly in older adults and patients with established CVD. Ectopic fat depots, such as epicardial and hepatic fat, further contribute to CV pathology through local and systemic mechanisms. Collectively, these findings highlight the limitations of BMI-centered approaches and support the integration of body composition measures into CV risk stratification. Emphasizing body recomposition, with reduction of harmful fat depots and preservation of skeletal muscle, may enable more precise, individualized strategies for CV prevention and management.

3,3'-Diindolylmethane ameliorate obesity-related skeletal muscle atrophy via regulating mitochondrial function.

Boosting muscle health in aging rats: The synergistic effect of vitamin C, silymarin, and endurance swimming on a high-fat diet.

Measuring the forces of individual muscles in a muscle group around a joint is non-trivial, and researchers have suggested using surrogates for individual muscle forces instead. Traditionally, experimentalists have shown that the force output of the skeletal muscle tissue can be correlated to the intra-muscular pressure (IMP) generated by the muscle belly. However, IMP proves difficult to measure in vivo, due to variations from sensor placement and invasiveness of the procedure. Numerical biomechanical simulations offer a tool to analyze muscle contractions, enabling new insights into the correlations among non-invasive experimentally measurable quantities, such as strains and the force output. In this work, we investigate the correlations between the muscle force output, the principal, shear and volumetric strains experienced by the muscle, as well as the pressure developed within the muscle belly as the tissue undergoes isometric contractions with varying activation profiles and magnitudes. It is observed that pressure does not correlate well with force output under higher sub-maximal and maximal activation levels, especially at locations away from the center of the muscle belly due to pressure relaxation effects. This study reveals strong correlations between force output and the strains at all locations of the belly, irrespective of the type of activation considered. This observation offers evidence for further in vivo studies using experimentally measurable principal and volumetric strains in the muscle belly as proxies for the force generation by the individual muscle and consequently enables the estimation on the contribution of various muscle groups to the total force.

Consumers' risky eating behaviours aided by the current food environment have led to an increase in diet-related metabolic disorders. Metabolic (dysfunction)-associated fatty liver disease origin represents a major global health burden that is increasing at an alarming rate on an annual basis. Modifying the timing of calorie consumption, dietary composition, or caloric intake offers a promising therapeutic approach for the management of this condition. The aim of this review was to provide a concise analysis of the impact of intermittent fasting on the regulation of glucocorticoid levels and diet-induced metabolic disorders with a focus on non-alcoholic fatty liver diseases. We found that intermittent fasting primarily regulates hepatic autophagy via nutritional and hormonal pathways, aiding in the maintenance of energy equilibrium, enhancement of mitochondrial function, regulation of liver quality, preservation of cellular homeostasis, protection of cells from harmful factors, mitigation of liver metabolic disorders, and improvement of liver inflammation. Also, the physiological changes induced by intermittent fasting and their metabolic consequences arise through multiple mechanisms, including alterations in hepatic metabolism, hepatic autophagy, inflammatory responses, liver functional enzymes, hepatic steatosis, fibroblast growth factor signalling, White adipoe tissue browning, adipokines, circadian rhythms, lipid profiles, body composition, the adipose tissue-gut microbiome axis, skeletal muscle, and the autophagy process. Interestingly, we identified the complex interplay among glucocorticoids, intermittent fasting, and non-alcoholic fatty liver diseases highlighting the hepatic macrophage glucocorticoid receptor as a pivotal mediator of fasting-induced reprogramming of the macrophage secretome, including fasting-suppressed cytokines. In conclusion, existing data indicates that intermittent fasting in patients with non-alcoholic fatty liver diseases is a viable, safe, and successful strategy for weight reduction, demonstrating notable trends in the amelioration of dyslipidaemia and non-alcoholic fatty liver diseases.

S100A11/ANXA2 axis mediates electrotransduction to promote electrically-induced contraction in engineered myocardial tissues.

Myoglobin in disease: the good and the bad.

Meticulous determination of the time since death (TSD) is critical in certain criminal investigations. This study aimed to identify optimal markers for TSD estimation and develop a mathematical model applicable under varying conditions. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and β-Actin (ACTB) mRNA levels were analyzed in 10 human skeletal muscle samples using real-time quantitative PCR at eight time intervals (6, 12, 18, 24, 30, 36, 42, and 48 h) within 48 h postmortem at 25°C. Among the candidate markers, GAPDH demonstrated the strongest correlation with times since death. At the same time, ACTB expression remained comparatively stable across all samples and time points as identified by RefFinder (reference gene analysis tool). Mathematical equations were developed using the Ct values for GAPDH, ACTB, and ΔCt (GAPDH-ACTB) and the cubic model gave the highest determination of coefficient while the error rates were low in the quadratic model. The findings indicate that ACTB is an optimal marker for estimating TSD within the 30 to 36-h postmortem interval, while GAPDH is more suitable for the 36 to 48-h period.