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Emerging studies have indicated that long non-coding RNAs (lncRNAs) play important roles in skeletal muscle growth and development. Nevertheless, it remains challenging to understand the function and regulatory mechanisms of these lncRNAs in muscle biology and associated diseases. Here, we identify a novel lncRNA, , that is significantly upregulated during myoblast differentiation and is highly expressed in skeletal muscle. We validated that promotes myoblast differentiation . Mechanistically, gives rise to mature microRNA (miR)-22-3p, which inhibits its target gene, histone deacetylase 4 (), thereby increasing the downstream myocyte enhancer factor 2C () and ultimately promoting myoblast differentiation. Furthermore, , we documented that knockdown delays repair and regeneration following skeletal muscle injury and further causes a significant decrease in weight following repair of an injured muscle. Additionally, gives rise to miR-22-3p to restrict expression, thereby promoting the differentiation and regeneration of skeletal muscle. Given the conservation of between mice and humans, might constitute a promising new therapeutic target for skeletal muscle injury, skeletal muscle atrophy, as well as other skeletal muscle diseases.
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http://dx.doi.org/10.1016/j.omtn.2021.02.025 | DOI Listing |
Am J Physiol Cell Physiol
September 2025
Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC.
Cachexia, the loss of skeletal muscle mass and function with cancer, contributes to reduced life quality and worsened survival. Skeletal muscle fibrosis leads to disproportionate muscle weakness; however, the role of infiltrating immune cells and fibro-adipogenic progenitors (FAPs) in cancer-induced muscle fibrosis is not well understood. Using the C26 model of cancer cachexia, we sought to examine the changes to skeletal muscle immune cells and FAPs which contribute to excessive extracellular matrix (ECM) collagen deposition.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
September 2025
Division of Medical Sciences, NOSM University, Ontario, Canada.
Cancer induced skeletal muscle wasting (cachexia) is responsible for over 20% of cancer related deaths, yet much about the pathophysiology of the condition remains unknown. Importantly, cancer cachexia does not seem wholly responsive to traditional anabolic stimuli such as nutritional interventions. It is possible that tumours directly or indirectly target skeletal muscle for their dynamic and abundant pool of amino acids that can be reliably used by tumours to supplement energy production and biomass synthesis.
View Article and Find Full Text PDFAm J Forensic Med Pathol
September 2025
Department of Pathology, St Louis University School of Medicine, Office of the Medical Examiner - City of St. Louis, St. Louis, MO.
Myotonic dystrophy type 1, or dystrophia myotonica type 1 (DM1), is a multisystem disorder inherited in an autosomal dominant manner. It is caused by a CTG tri-nucleotide expansion in the 3'-untranslated region (3'-UTR) of the dystrophia myotonia protein kinase (DMPK) gene. Core clinical features include progressive skeletal muscle weakness, myotonia, and systemic complications, with premature mortality most often due to respiratory or cardiac dysfunction.
View Article and Find Full Text PDFNeuropathol Appl Neurobiol
October 2025
Division of Rheumatology and Systemic Inflammatory Diseases, III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Aims: Sarcoid myopathy (SaM) is characterised by granulomatous myositis (GM) and can overlap with inclusion body myositis (IBM), a late-onset chronic idiopathic inflammatory myopathy with a still enigmatic pathogenesis. As GM can occur in different clinical contexts, we aimed to examine the histomorphologic features and gene expression profiles in cases of definite SaM that may inform diagnostic and therapeutic considerations.
Methods: We performed a multidimensional characterisation of muscle biopsy specimens from patients with 'pure SaM' (n=17), SaM with concomitant IBM (SaM-IBM) (n=2), including histopathologic and ultrastructural analysis in addition to quantitative real-time polymerase chain reaction.
J Cachexia Sarcopenia Muscle
October 2025
Department of Sports Science, College of Natural Science, Jeonbuk National University, Jeonju, Republic of Korea.
Background: Fine particulate matter has developmental toxicity, and midgestation is an important period for the development of foetal skeletal muscle. The ability of exercise to modulate skeletal muscle damage in mice exposed to PM during gestation remains unclear.
Methods: Pregnant C57BL/6 mice were exposed to 50 μg/m PM for 2 h on five consecutive days starting at embryonic day 12.