Ginkgetin alleviates cisplatin-induced muscle atrophy via inhibition of the macrophage cGAS-STING pathway.

Neuromuscular junction dysfunction in a subset of Charcot-Marie Tooth and related peripheral neuropathies mouse models.

Data on the manifestation and progression of neurological and psychiatric symptoms in adult patients with late-onset Tay-Sachs (LOTS) disease after the age of 2years are scarce and not available for Germany. In this cross-sectional study data from the "8 in 1" register study for gangliosidoses of 16 adult patients with LOTS were retrospectively evaluated with respect to the manifestation and the occurrence of neurological and psychiatric symptoms. The LOTS can be manifested in preschool age with aneurodevelopmental disorder, in school age and adolescence with cerebellar symptoms or in adolescence and adulthood with leg dominant muscle weakness and muscle atrophy in the sense of a motor neuron disease (MND). The initial symptoms of LOTS begin insidiously, are variable and often go unrecognized. Severe psychiatric disorders regularly occur in the course of the disease, particularly in those patients who have neurological developmental disorders and manifestation of cerebellar symptoms. The prevalence of psychiatric disorders is 62.5%. In 10 of the 16adult patients, psychoses occurred that were diagnosed as severe depression, bipolar affective disorder, as polymorphic psychotic disorder or as schizoaffective disorder. The patients were treated in particular with atypical antipsychotic drugs, benzodiazepines and mood stabilizers. Neuropsychiatric symptoms in LOTS were explained with the concept of a cerebellar cognitive affective syndrome (CCAS) as an organic brain disease of the cerebellum; however, symptoms such as massive psychomotor agitation, anxiety, rapid mood swings, confusion, formal and content-related thought disorder as well as hallucinations cannot be completely explained by CCAS and are consistent with concepts that describe a role of cerebellar network dysfunctions in psychoses. Our data can help to include LOTS as adifferential diagnosis in patients with psychiatric and neurological symptoms.

A novel cosmetic vascularized bone flap craniotomy for postauricular transmastoid approach for jugular foramen tumors.

Skeletal muscle undergoes progressive denervation-induced muscle atrophy (DIMA) after peripheral nerve injury that severely impairs the potential for motor functional recovery with reinnervation. There are currently no therapeutic strategies to reverse the deleterious effects of chronic DIMA, leaving affected patients with lifelong disability. Herein, we used a translational rodent forelimb nerve injury model to investigate whether targeted injection of syngeneic myoblasts to chronically atrophic muscle can reverse the histologic and functional consequences of DIMA. Male Lewis rats underwent median nerve transection followed by immediate (positive control) or delayed repair. Following a plateau of motor function, myoblasts were injected into the digital flexor muscles (n = 5-6 per group), delivered in either saline or a nanofiber hydrogel composite (NHC) loaded with agrin- and insulin-like growth factor 1 (IGF-1)-releasing nanoparticles (npNHC). Serial functional assessments of stimulated grip strength and terminal histological evaluation were used to measure recovery. Satellite cell-rich (Pax7 Hi ) myoblast therapy caused sustained improvement in stimulated grip strength from pretreatment baseline (p < 0.05). Histological evaluation demonstrated that myoblast therapy, when delivered in npNHC, reversed whole muscle atrophy compared to positive controls [p = 0.997 and 0.996] and restored mean myofiber cross-sectional area [p = 0.244]. Correlation analysis demonstrated functional improvements were associated with increased myofiber cross-sectional area [r = 0.900, p = 3.01E-09]. This data indicates that targeted injection of syngeneic myoblasts can reverse the functional and histologic effects of DIMA in skeletal muscles and is a promising strategy for improving recovery after peripheral nerve injuries.

Skeletal Muscle Mass and Quality in Peripheral Artery Disease: New Insights into Clinical Management and Therapeutic Optimization.

Advancements in Prenatal Diagnosis and Potential Fetal Therapies for Spinal Muscular Atrophy.

Post-polio syndrome (PPS) is characterized by progressive muscle weakness and atrophy decades after acute poliomyelitis. While muscle involvement is typically asymmetric and patchy, specific patterns of selective muscle sparing have not been well characterized. We report two male patients (ages 36 and 69 years) with a remote history of paralytic poliomyelitis who presented with progressive lower limb weakness and atrophy, fulfilling the March of Dimes diagnostic criteria for PPS. Detailed clinical examination revealed asymmetric motor deficits with right-sided predominance. Comprehensive electrophysiological studies demonstrated chronic neurogenic changes without evidence of active denervation or upper motor neuron involvement. Muscle MRI of the thighs revealed a progressive pattern of selective muscle sparing: Patient 1 demonstrated unilateral preservation of the sartorius and biceps femoris in the newly affected left thigh, with end-stage fatty obliteration of these muscles in the previously affected right thigh; Patient 2 demonstrated bilateral preservation of these muscles, representing an earlier stage of the same pathophysiological process. This observation suggests that post-polio muscular degeneration follows a hierarchic and progressive pattern. The sartorius and biceps femoris exhibit relative resilience-delayed rather than absolute resistance to degeneration-possibly reflecting unique anatomical, developmental, or pathophysiological protective factors. This MRI pattern may serve as a dynamic imaging clue to support PPS diagnosis and stage assessment, though validation in larger cohorts is required.

Peripheral nerve injury (PNI) remains a major regenerative challenge, in part because the post-injury microenvironment can disrupt Schwann cell (SCs) homeostasis. Walnuts (Juglans regia) have long been used in ethnomedicine for perceived neurotrophic or neuroprotective benefits, a view historically linked to their resemblance to the brain. To examine whether this traditional concept can be leveraged as a nanotherapeutic approach, we isolated walnut-derived extracellular vesicles (WEVs) and evaluated their effects on peripheral nerve repair. We found that WEVs are readily internalized by SCs and can help establish a "pre-regenerative niche," defined here as a permissive metabolic microenvironment that supports repair. Mechanistically, WEVs appear to engage a c-Myc-mediated transcriptional program that shifts SC metabolism toward aerobic glycolysis and increases lactate export, consistent with activation of a glia-to-neuron lactate shuttle. In parallel, WEVs may stabilize the glial bioenergetic hub by limiting stress-induced mitophagy. In a rat sciatic nerve compression model, these changes were associated with preserved mitochondrial ultrastructure in the acute phase, followed by enhanced remyelination, improved motor and sensory outcomes, and attenuated muscle atrophy. Collectively, our findings suggest a mechanistic basis for the reported neuroprotective value of walnuts and identify WEVs as a niche-modulating nanotherapeutic candidate that may promote regeneration by aligning glial metabolic plasticity with neuronal energy demands.

Molecular mechanisms of skeletal muscle atrophy: clinical challenges and future therapeutic strategies.

Hyperoside accelerates myelin debris clearance by inhibiting signal transducer and activator of transcription 3 phosphorylation in peripheral nerve injury.

Skeletal muscle is a highly adaptable tissue that plays a central role in overall health. The dynamic balance between muscle protein synthesis and breakdown governs skeletal muscle mass maintenance. Increased loading and hyperaminoacidemia (via protein ingestion) are positive drivers of skeletal muscle protein accretion, which, when combined, drive a hypertrophic phenotypic adaptation. In contrast, unloading (disuse) results in skeletal muscle atrophy and metabolic dysregulation. Hypertrophy enhances metabolic health and functional capacity, underscoring the importance of understanding the mechanisms that regulate this process. External variables, such as resistance exercise and dietary protein, influence hypertrophy; however, resistance exercise is the primary driver, with protein playing a minor supporting role. Signals from external input loading (resistance exercise) and nutritional manipulation (protein ingestion) are sensed and transduced into intracellular pathways that promote muscle protein synthesis, yet the precise mechanisms underlying their integration remain incompletely understood. This review summarizes current knowledge on how resistance exercise and dietary protein converge on the intracellular level to regulate skeletal muscle hypertrophy in humans.

Skeletal muscle (SkM) atrophy is an associated disorder of cachexia, sarcopenia, immobilization, and denervation and is responsible for increased mortality and morbidity. SkM atrophy is often characterized by increased protein degradation and decreased protein synthesis in skeletal muscle. Increased protein catabolism is firmly associated with protein ubiquitination, an associated post-transcriptional modification of proteins that mediate diverse cellular functions like cell growth, cell death, DNA damage repair, and protein degradation. During the SkM atrophy, the extents of ubiquitination decide the degradative pathway of proteins as well as organelles. The ubiquitination process is regulated by three enzymes, ubiquitin-activating enzyme (E1), ubiquitin-conjugating enzyme (E2), and an E3 ubiquitin ligase (E3) to mediate the transfer of ubiquitin to the Lys residue of the targeted protein. More than 600 E3 ligases (Reviewed Uniprot Database) known to date are tissue-specific, organ-specific, and ubiquitous. Hence, E3 ligases may be selective drug targets due to their involvement in the regulation of stabilities and functions of proteins. Muscle atrophy F-box protein (MAFbx)/atrogin-1, and E3 ubiquitin-protein ligase TRIM63 (MuRF-1) are highly explored muscle-specific E3 ligases. However, the inhibition of MAFbx and MuRF-1 cannot stop the muscle atrophy completely. Hence, the involvement of other highly expressed E3 ubiquitin-protein ligases in SkM i.e., TRIM7, UBE2O, MIB2, and CHIP are also important factors in SkM atrophy. Hence, this review aimed to highlight the interplay and importance of E3 ligases in SkM atrophy.

BackgroundSarcopenia is a progressive skeletal muscle disorder associated with increased disability, morbidity, and mortality. Ultrasound has gained increasing attention as an accessible and repeatable tool for muscle assessment.ObjectiveThis study aimed to map the global research trends and technological evolution in ultrasound-based sarcopenia assessment from 1997 to 2025.MethodsA total of 1574 records were retrieved from the Web of Science Core Collection. Bibliometric analyses were performed using CiteSpace, VOSviewer, and the bibliometrix R package. Sankey diagrams were used to visualize thematic flows between ultrasound assessment dimensions and outcome-related research topics.ResultsPublications showed a prolonged latent phase, steady growth, and rapid acceleration after 2019, peaking in 2025. Keyword and thematic-flow analyses identified a three-stage evolution: an early Morphometry Phase centered on muscle size and atrophy, a Qualitative Transition Phase emphasizing muscle quality and chronic disease contexts, and an Advanced Functional and AI Phase characterized by elastography, AI-assisted analysis, and outcome-related topics. Research contexts expanded across geriatrics, nephrology, critical care, surgical oncology, and rehabilitation-related research.ConclusionUltrasound-based sarcopenia research has shifted toward multidimensional muscle assessment and technology-assisted analysis. Because this study did not appraise individual study quality or clinical effect sizes, the findings should be interpreted as bibliometric patterns and research priorities rather than direct evidence of diagnostic or prognostic effectiveness.

ZBP1 deficiency ameliorates the motor dysfunction following brachial plexus root avulsion in mice.

Preservation of skeletal muscle mass and function is a key feature of healthy ageing and relies on the tight coordination between protein synthesis and breakdown to maintain proteostatic balance. These processes impose a substantial energetic demand, highlighting the importance of mitochondrial function in skeletal muscle homeostasis. Increasing evidence indicates that mitochondria and the sarcoplasmic reticulum are functionally interconnected. Effective crosstalk between these organelles contributes to the integration of bioenergetic supply, Ca²⁺ handling, and proteostasis. Disruption of this communication network may impair adaptive stress responses, compromise protein quality control, and favour the development of anabolic resistance during ageing. This review synthesizes current evidence on mitochondria-sarcoplasmic reticulum communication. It further discusses how disruption of this crosstalk may promote anabolic resistance and skeletal muscle atrophy, with particular emphasis on its implications for age-related muscle decline.

Cisplatin is a commonly used chemotherapeutic agent for the treatment of diverse malignancies; however, its clinical use often results in skeletal muscle atrophy (SMA). Excessive generation of reactive oxygen species (ROS) and persistent unsettled inflammation are significant contributors to cisplatin (CPT)-induced skeletal muscle atrophy (CiSMA). Nanoparticles capable of scavenging ROS and alleviating inflammation may effectively address CiSMA. We developed a straightforward, fast one-step method for fabricating tailored zinc-polydopamine (Zn-PD) nanozymes and confirmed their promising therapeutic agents for CiSMA. Zn-PD, which exhibits diverse enzyme-mimicking capabilities, Zn-PD effectively inhibits ROS-triggered myotube apoptosis, rectifies mitochondrial dysfunction, and enhances mitochondrial biogenesis, demonstrating significant anti-inflammatory effects by obstructing the M1 macrophage infiltration into the muscle milieu, thereby mitigating CiSMA in mice. Collectively, this study proposes a treatment approach for CiSMA and underscores the potential of Zn-PD-based therapies for treating muscle atrophy during the perioperative period of surgery.

The chemotherapeutic agent cisplatin for solid tumors frequently induces cancer-associated cachexia characterized by weight loss and decreased skeletal muscle mass. These adverse cisplatin-related symptoms are dose‑limiting, and the ability to counteract drug-initiated muscle atrophy in cancer-associated cachexia remains a pharmacological challenge. The aim of this study was to determine the protective efficacy of lobetyolin, a natural compound derived from Codonopsis pilosula, known to exert antioxidant, anti‑inflammatory, and anti‑apoptotic activities, against cisplatin-induced skeletal muscle wasting and subsequently elucidate a potential underlying molecular mechanism of action using a mouse model. Mice were injected with cisplatin (4 mg/kg, i.p. every other day, 4 doses in total) with concurrent oral lobetyolin (20 or 40 mg/kg daily) for 8 days. Lobetyolin inhibited cisplatin-induced reductions in body weight and grip strength, ameliorated gastrocnemius muscle atrophy, and preserved myofiber cross‑sectional area. Mechanistically, lobetyolin restored superoxide dismutase (SOD) activity and glutathione (GSH) levels while diminishing malondialdehyde (MDA) content in gastrocnemius muscle. Lobetyolin was found to activate the AKT signaling axis as evidenced by enhanced phosphorylation of AKT (Ser473) and FoxO3α (Thr32), which suppressed FoxO3α nuclear translocation and downregulated the E3 ubiquitin ligase Fbx32, thereby diminishing proteasomal protein degradation. Concurrently, lobetyolin normalized the Bax/Bcl‑2 ratio to inhibit myocyte apoptosis. These findings demonstrated that lobetyolin may be considered as a multi‑targeted therapeutic candidate to counteract oxidative injury, protein catabolism, and myocyte apoptosis initiated by cisplatin. Data suggest that lobetyolin's potential as a safe adjunctive agent against chemotherapy‑induced muscle wasting might involve AKT/FoxO3α pathway.

Squalene Alleviates Cancer Cachexia-Induced Muscle Atrophy and Adipose Tissue Wasting in CT26 Tumor-Bearing Mice.

Skeletal muscle wasting is a serious complication of chronic kidney disease (CKD) and is associated with increased mortality. However, the main determinants of muscle atrophy in CKD are not yet well known and may differ in the general and CKD populations. The aim of this study was to investigate the relationships between appendicular skeletal muscle mass (ASM) and anthropometric measurements, body composition parameters as well as laboratory results, and compare these associations in patients with estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73 m2 and participants with eGFR ≥ 60 ml/min/1.73 m2. Two groups of male participants were included: 33 patients with eGFR < 60 ml/min/1.73 m2 and 38 individuals with eGFR ≥ 60 ml/min/1.73 m2. Muscle mass and body composition variables, including ASM, were assessed by bioimpedance spectroscopy (BIS). Blood samples were taken to evaluate serum creatinine, urea, haemoglobin, C-reactive protein (CRP) and albumin. In both groups of patients ASM positively correlated with body mass, body mass index (BMI), lean tissue mass (LTM) and lean tissue indx (LTI) (p < 0.05 for all parameters). ASM positively correlated with height in individuals with eGFR ≥ 60 ml/min/1.73 m2 (p = 0.001). There was no statistically significant correlations between laboratory parameters and ASM in both groups. ASM is associated significantly and positively with anthropometric and body composition parameters such as body mass, BMI, LTM and LTI both in patients with eGFR < 60 ml/min/1.73 m2 and in those with eGFR ≥ 60 ml/min/1.73 m2 which suggests that the determinants of ASM are similar in CKD and in the general population.