Muscle degeneration and myopathies encompass a range of conditions characterized by the progressive loss of muscle mass and function. Recent studies have identified various molecular pathways that contribute to muscle wasting, particularly in the context of cancer cachexia. For instance, Angelino et al. demonstrated that impaired cAMP-PKA-CREB1 signaling leads to mitochondrial dysfunction in skeletal muscle during cancer cachexia, highlighting the potential of targeting PDE4D as a therapeutic strategy (ref: Angelino doi.org/10.1038/s42255-025-01397-5/). Similarly, Joshi et al. found that the IRE1α/XBP1 pathway plays a critical role in mediating muscle wasting during pancreatic cancer cachexia, suggesting that interventions aimed at this pathway could mitigate muscle loss (ref: Joshi doi.org/10.1038/s44321-025-00337-w/). Furthermore, McGowan et al. explored the role of laminin-α12 in LAMA2-related muscular dystrophy, revealing that its absence leads to muscle stem cell dysfunction, which is crucial for maintaining muscle integrity (ref: McGowan doi.org/10.1038/s41467-025-65703-1/). These findings collectively emphasize the importance of understanding the underlying molecular mechanisms to develop effective treatments for muscle degeneration. In addition to cancer-related muscle wasting, other studies have focused on the effects of chemotherapy on muscle health. Isesele et al. investigated the protective effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) against chemotherapy-induced myotoxicity, demonstrating that these omega-3 fatty acids can attenuate muscle loss (ref: Isesele doi.org/10.1002/jcsm.70110/). Moreover, research by Hermitte et al. highlighted the significance of alternative splicing of SORBS1 in myotonic dystrophy type 1, linking splicing misregulation to neuromuscular junction integrity (ref: Hermitte doi.org/10.1002/jcsm.70112/). The interplay of these various factors underscores the complexity of muscle degeneration and the need for multifaceted therapeutic approaches.

Inflammatory myopathies, particularly idiopathic inflammatory myopathy (IIM), present significant clinical challenges due to their heterogeneous nature and association with autoimmunity. Recent studies have explored the relationship between myositis-specific autoantibodies (MSA) and clinical features in IIM patients. Li et al. found that anti-MDA5 positive patients exhibited shorter disease duration and higher rates of associated symptoms such as rash and interstitial lung disease (ILD), while anti-ARS positive patients had a longer disease duration but better prognosis (ref: Li doi.org/10.3389/fimmu.2025.1674437/). This highlights the importance of autoantibody profiling in predicting disease outcomes and tailoring treatment strategies. Furthermore, the prognostic implications of MSAs were further elucidated by Hou et al., who reported that patients with anti-TIF1-γ and anti-MDA5 antibodies faced higher mortality risks, while anti-Mi-2 and anti-NXP2 patients had increased relapse rates (ref: Hou doi.org/10.1111/ene.70446/). Zhu et al. introduced the LOCCM index as a predictive biomarker for progressive pulmonary fibrosis in anti-synthetase syndrome, demonstrating its strong predictive power (ref: Zhu doi.org/10.1186/s12931-025-03414-3/). These findings emphasize the critical role of biomarkers in assessing disease severity and guiding therapeutic interventions in inflammatory myopathies.

Mitochondrial dysfunction is a central feature in various muscle disorders, contributing to muscle degeneration and impaired function. Scalabrin et al. investigated the interplay between peroxisomes and mitochondria in skeletal muscle, revealing that alterations in peroxisome function can accelerate muscle dysfunction (ref: Scalabrin doi.org/10.1038/s41467-025-64833-w/). This study underscores the importance of understanding organelle interactions in the context of muscle health and disease. Additionally, Joshi et al. highlighted the role of the IRE1α/XBP1 pathway in mediating muscle wasting during pancreatic cancer cachexia, further linking mitochondrial dysfunction to cancer-related muscle loss (ref: Joshi doi.org/10.1038/s44321-025-00337-w/). Moreover, Aremu et al. demonstrated that N-acetylcysteine (NAC) can prevent cisplatin-induced skeletal muscle atrophy by inducing myogenic microRNAs and maintaining redox balance, suggesting potential therapeutic avenues for mitigating chemotherapy-induced muscle damage (ref: Aremu doi.org/10.3390/antiox14111344/). Nascimento et al. also reported that hydroethanolic soy extract rich in isoflavones protects dystrophic mutant mice from oxidative stress and inflammation, indicating that dietary interventions may offer protective benefits against mitochondrial dysfunction in muscle disorders (ref: Nascimento doi.org/10.1002/biof.70062/). Collectively, these studies highlight the multifaceted role of mitochondrial dysfunction in muscle disorders and the potential for targeted therapies.

The genetic landscape of myopathies has expanded significantly with advances in genomic technologies, revealing a multitude of genetic variants associated with muscle disorders. Di Feo et al. conducted a comprehensive analysis of TTN variants in a large cohort, emphasizing the challenges in interpreting the clinical significance of these variants given their prevalence in the general population (ref: Di Feo doi.org/10.1016/j.gim.2025.101649/). This study underscores the need for robust frameworks to assess the pathogenicity of genetic variants in myopathy. In addition, Kim et al. explored the loss of adenylosuccinate synthetase 1 in mice, which recapitulates features of ADSS1 myopathy, providing insights into the metabolic pathways involved in muscle degeneration (ref: Kim doi.org/10.1093/hmg/). Akyürek et al. investigated the potential of CFTR corrector C17 to rescue defective SERCA1 in bovine pseudomyotonia, suggesting novel therapeutic strategies for Brody myopathy (ref: Akyürek doi.org/10.1093/hmg/). These findings highlight the intricate genetic and molecular mechanisms underlying myopathies, paving the way for targeted genetic therapies.

Therapeutic interventions for myopathies have gained traction as researchers explore various strategies to improve muscle function and mitigate disease progression. Andreasson et al. conducted a randomized controlled trial comparing high-intensity interval training (HIIT) to moderate exercise in patients with recent-onset idiopathic inflammatory myopathies, finding that HIIT significantly improved aerobic capacity and muscle endurance (ref: Andreasson doi.org/10.1016/j.ebiom.2025.106051/). This study highlights the potential of exercise interventions in enhancing muscle function in myopathy patients. Additionally, Yang et al. identified interleukin-33 as a promoter of interstitial lung disease in IIM, suggesting that targeting this pathway may provide new therapeutic options for managing lung complications associated with myopathy (ref: Yang doi.org/10.1002/art.43453/). Lad et al. further explored the pathogenic influences of autoantibodies in immune-mediated necrotizing myopathy, revealing that these antibodies can directly impair muscle contractile function, indicating the need for targeted immunotherapies (ref: Lad doi.org/10.1186/s13395-025-00400-7/). These studies collectively emphasize the importance of innovative therapeutic approaches in managing myopathies and improving patient outcomes.

Exercise and rehabilitation play a crucial role in managing muscle disorders, with recent studies demonstrating the efficacy of various exercise modalities. Andreasson et al. highlighted the benefits of high-intensity interval training (HIIT) in patients with recent-onset idiopathic inflammatory myopathies, showing a significant improvement in aerobic capacity and muscle endurance compared to moderate exercise (ref: Andreasson doi.org/10.1016/j.ebiom.2025.106051/). This finding underscores the potential of tailored exercise programs to enhance muscle function and overall health in myopathy patients. Moreover, Catinelli et al. investigated the effects of swimming exercise on diabetic myopathy in pregnant rats, revealing that exercise can reverse muscle degeneration and promote histological and mitochondrial adaptations (ref: Catinelli doi.org/10.1016/j.bbadis.2025.168126/). These findings suggest that exercise not only improves muscle function but also induces beneficial changes at the cellular level. Furthermore, studies on dietary interventions, such as fish oil supplementation, have shown promise in mitigating exercise-induced muscle damage, indicating that a multifaceted approach combining exercise and nutrition may optimize rehabilitation outcomes in muscle disorders (ref: Lee doi.org/10.3390/nu17213408/).

Clinical assessment and the identification of biomarkers are critical for diagnosing and managing myopathies. Zhu et al. developed the LOCCM index, a serum biomarker-based tool for predicting progressive pulmonary fibrosis in patients with anti-synthetase syndrome, demonstrating its strong predictive power (ref: Zhu doi.org/10.1186/s12931-025-03414-3/). This highlights the importance of biomarkers in guiding clinical decision-making and monitoring disease progression. Additionally, Hou et al. examined the prognostic implications of myositis-specific autoantibodies in dermatomyositis patients, revealing that certain autoantibodies are associated with higher risks of mortality and relapse (ref: Hou doi.org/10.1111/ene.70446/). These findings emphasize the need for comprehensive autoantibody profiling in clinical practice to tailor treatment strategies effectively. Furthermore, Nezamdoust et al. addressed the social and medical marginalization of patients with severe chronic fatigue syndrome, shedding light on the broader implications of myopathy-related conditions and the necessity for inclusive healthcare approaches (ref: Nezamdoust doi.org/10.1016/j.socscimed.2025.118766/). Collectively, these studies underscore the significance of clinical assessments and biomarkers in enhancing the management of myopathies.

Environmental and lifestyle factors significantly influence muscle health and the progression of muscle disorders. Recent studies have explored the impact of dietary interventions and exercise on muscle function. Catinelli et al. demonstrated that swimming exercise can attenuate diabetic myopathy in pregnant rats, highlighting the role of physical activity in reversing muscle degeneration and promoting mitochondrial health (ref: Catinelli doi.org/10.1016/j.bbadis.2025.168126/). This suggests that exercise can serve as a therapeutic strategy for managing muscle disorders associated with metabolic conditions. Additionally, Lee et al. investigated the effects of acute fish oil supplementation on muscle function following exercise-induced muscle damage, finding that it may mitigate muscle soreness and enhance recovery (ref: Lee doi.org/10.3390/nu17213408/). Similarly, Gurton et al. examined the effects of sodium bicarbonate on functional recovery after exercise-induced muscle damage, demonstrating its potential to improve performance in athletes (ref: Gurton doi.org/10.3390/nu17213383/). These findings emphasize the importance of integrating lifestyle modifications, including diet and exercise, into the management of muscle health and disorders.