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Melittin, a honeybee venom derived peptide for the treatment of chemotherapy-induced peripheral neuropathy.

Chemotherapy-induced peripheral neuropathy (CIPN) is the most prevalent neurological complication of cancer treatment which involves sensory and motor nerve dysfunction. Severe CIPN has been reported in around 5% of patients treated with single and up to 38% of patients treated with multiple chemotherapeutic agents. Present medications available for CIPN are the use of opioids, nonsteroidal anti-inflammatory agents, and tricyclic antidepressants, which are only marginally effective in treating neuropathic symptoms. In reality, symptom reappears after these drugs are discontinued. The pathogene

Amiloride ameliorates muscle wasting in cancer cachexia through inhibiting tumor-derived exosome release.

BACKGROUND: Cancer cachexia (CAC) reduces patient survival and quality of life. Developments of efficient therapeutic strategies are required for the CAC treatments. This long-term process could be shortened by the drug-repositioning approach which exploits old drugs approved for non-cachexia disease. Amiloride, a diuretic drug, is clinically used for treatments of hypertension and edema due to heart failure. Here, we explored the effects of the amiloride treatment for ameliorating muscle wasting in murine models of cancer cachexia. METHODS: The CT26 and LLC tumor cells were subcutaneously in

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… C2C12 myoblasts were cultured to 85–90% confluence in DMEM growth medium. Myoblast differentiation was induced by incubation for 96 h in DMEM supplemented with 2% heat-inactivated horse serum. C2C12 myoblasts were used within ten generations of culture. …

Clinical management and therapeutic development for the rare disease rhabdomyosarcoma.

Rhabdomyosarcoma (RMS) is a rare disease that arises from skeletal muscle mainly affects children and adolescents. Patients with RMS have diverse symptoms and prognosis based on tumor sizes, tumor anatomical locations, histological subtypes of the tumors and genetic testing of paired-box-forkhead box O1 (PAX-FOXO1) fusion gene. The 4 subtypes of RMS include embryonal RMS (eRMS), alveolar RMS (aRMS), spindle cell/sclerosing RMS (scRMS) and pleomorphic RMS (pRMS). Treatment for RMS patients remains challenging due to its heterogeneous nature. Thus, a combinatory approach is likely to warrant bet

Safety and Efficacy of Givinostat for Patients with Muscular Dystrophy: A Systematic Review.

INTRODUCTION: Muscular dystrophy (MD) refers to a group of genetic disorders leading to progressive weakness and degeneration of skeletal muscle. Among them, Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are the most common types. Histone deacetylase inhibitors (i.e., givinostat) is a recently approved therapy for DMD. In this systematic review, we aimed to evaluate givinostat in MD patients regarding safety and efficacy. METHODS: A systematic review was performed according to the PRISMA guidelines by searching through Medline, Embase, Cochrane Library, and Web of Scie

Exosomes to exosome-functionalized scaffolds: a novel approach to stimulate bone regeneration.

Bone regeneration is a complex biological process that relies on the orchestrated interplay of various cellular and molecular events. Bone tissue engineering is currently the most promising method for treating bone regeneration. However, the immunogenicity, stable and cell quantity of seed cells limited their application. Recently, exosomes, which are small extracellular vesicles released by cells, have been found to effectively address these problems and better induce bone regeneration. Meanwhile, a growing line of research has shown the cargos of exosomes may provide effective therapeutic an

Molecular and cellular mechanisms of skeletal muscle atrophy: an update.

Skeletal muscle atrophy is defined as a decrease in muscle mass and it occurs when protein degradation exceeds protein synthesis. Potential triggers of muscle wasting are long-term immobilization, malnutrition, severe burns, aging as well as various serious and often chronic diseases, such as chronic heart failure, obstructive lung disease, renal failure, AIDS, sepsis, immune disorders, cancer, and dystrophies. Interestingly, a cooperation between several pathophysiological factors, including inappropriately adapted anabolic (e.g., growth hormone, insulin-like growth factor 1) and catabolic pr

Effects of Physical Cues on Stem Cell-Derived Extracellular Vesicles toward Neuropathy Applications.

The peripheral nervous system undergoes sufficient stress when affected by diabetic conditions, chemotherapeutic drugs, and personal injury. Consequently, peripheral neuropathy arises as the most common complication, leading to debilitating symptoms that significantly alter the quality and way of life. The resulting chronic pain requires a treatment approach that does not simply mask the accompanying symptoms but provides the necessary external environment and neurotrophic factors that will effectively facilitate nerve regeneration. Under normal conditions, the peripheral nervous system self-r

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… Naskar et al. applied a direct current (DC) of low-level ES of ~8 ± 0.06 mV/mm for 20 h/day for nine days to a hMSC and murine myoblast coculture within a microfluidic device [ 287 ]. … The condition media also facilitated exosome mRNA protein translation from differentiated neural hMSCs to the myoblasts, exhibiting neural-like phenotypes and morphology [ 287 ]. …

The Role of Extracellular Vesicles (EVs) in the Epigenetic Regulation of Bone Metabolism and Osteoporosis.

Extracellular vesicles (EVs) are complex phospholipidic structures actively released by cells. EVs are recognized as powerful means of intercellular communication since they contain many signaling molecules (including lipids, proteins, and nucleic acids). In parallel, changes in epigenetic processes can lead to changes in gene function and finally lead to disease onset and progression. Recent breakthroughs have revealed the complex roles of non-coding RNAs (microRNAs (miRNAs) and long non-coding RNAs (lncRNAs)) in epigenetic regulation. Moreover, a substantial body of evidence demonstrates tha

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… When they overexpressed miR-34a in mouse myoblast C2C12 cells by lentiviral vector infection and induced miR-34a human primary myotubes by hydrogen peroxide treatment (to simulate oxidative stress), the cells released EVs enriched in miR-34a, which in turn were able to abrogate Sirtuin 1 ( sirt1 ). … | miR-34a | Bone marrow stromal cells | Induction of Sirtuin 1 reduction and senescence in bone marrow stromal cells | [ 143 ] Myoblasts | Myostatin/miR-218 | Osteocytic cells Ocy454 | Decrease in osteocytic miR-218 leading to an increase in RANKL expression and decrease in SOST. | [ 147 ] 6. …

Emerging Research and Future Directions on Doxorubicin: A Snapshot.

Doxorubicin, a widely used anthracycline antibiotic, has been a cornerstone in cancer chemotherapy since the 1960s. In addition to doxorubicin, anthracycline chemotherapy medications include daunorubicin, idarubicin, and epirubicin. For many years, doxorubicin has been the chemotherapy drug of choice for treating a broad variety of cancers. Despite its efficacy, doxorubicin therapy is hindered by serious side effects, primarily cardiotoxicity, and the challenges of drug resistance. Recent research has focused on optimizing doxorubicin's therapeutic index by developing cardioprotective strategi

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… L’Ecuyer et al, demonstrated in H9C2 cardiac myoblasts that the reduction of oxidative stress-induced activation of the DNA damage pathway and consequent cell death by mild hypothermia supports a possible protective role to reduce the clinical impact of DOX-induced cardiac toxicity [63]. … Effect of hypothermia on doxorubicin-induced cardiac myoblast signaling and cell death. Cardiovasc Pathol. 2012;21(2):96–104. doi: 10.1016/j.carpath.2011.02.001. 64. Zhang X, Xu B, Ni J, Xiang Y, He Z. …

Modulation of angiogenesis with siRNA inhibitors for novel therapeutics.

Cancer and many other serious diseases are characterized by the uncontrolled growth of new blood vessels. Recently, RNA interference (RNAi) has reinvigorated the therapeutic prospects for inhibiting gene expression and promises many advantages over binding inhibitors, including high specificity, which is essential for targeted therapeutics. This article describes the latest developments using small-interfering RNA (siRNA) inhibitors to downregulate various angiogenic and tumor-associated factors, both in cell-culture assays and in animal disease models. The majority of research efforts are cur

p38 MAPK regulates the Wnt inhibitor Dickkopf-1 in osteotropic prostate cancer cells.

The Wnt inhibitor Dickkopf-1 (DKK-1) has been associated with the occurrence of bone metastases in osteotropic prostate cancer by inhibiting osteoblastogenesis. P38 mitogen-activated protein kinase (MAPK) activity is also dysregulated in advanced prostate cancer. However, the impact of p38 MAPK signaling on DKK-1 remains unknown. Inhibition of p38 MAPK signaling in osteolytic PC3 cells by small molecule inhibitors (doramapimod, LY2228820 and SB202190) suppressed DKK-1 expression, whereas activation of p38 MAPK by anisomycin increased DKK-1. Further dissection by targeting individual p38 MAPK i

Перепрофилированный активатор Nrf2 диметилфумарат спасает мышцы воспаление и фиброз в отягченной мышиной модели мышечной дистрофии Дученна.

В унаследованных нейромускульных болезнях мышечная дистрофия Дюченна (ДМД) глюкокортикоиды значительно медленнее прогрессируют, но в то же время создают достаточно серьезные побочные эффекты, исключающие применение в значительной части пациентов. Распространяя наши выводы о том, что в результате острого лечения с УЛХ были одобрены многочисленные склерозные препараты, диметилфумарат (ДМФ), спасающая мышечную патологию у молодых мышей Mdx, мы намеревались провести доклиническое тестирование на перевод. Чтобы усилить фенотип болезни у взрослых мышц mdx, у которых обычно нет эквивалентной человече

Kabuki Syndrome-Clinical Review with Molecular Aspects.

Kabuki syndrome (KS) is a rare developmental disorder principally comprised of developmental delay, hypotonia and a clearly defined dysmorphism: elongation of the structures surrounding the eyes, a shortened and depressed nose, thinning of the upper lip and thickening of the lower lip, large and prominent ears, hypertrichosis and scoliosis. Other characteristics include poor physical growth, cardiac, gastrointestinal and renal anomalies as well as variable behavioral issues, including autistic features. De novo or inherited pathogenic/likely pathogenic variants in the KMT2D gene are the most c

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… KMT2D and KDM6A proteins regulate the differentiation of mesenchymal cell lineages: myoblasts and osteoblasts. Mouse models have shown that lysine demethylase plays a crucial role in regulating mesenchymal lineage cell differentiation. … KMT and lysine demethylase proteins’ specific role in the regulation of myoblast differentiation was also recently examined using the C2C12 myoblast model system. KDM1A is the only one crucial for myogenic differentiation, while KDM6A (among others) is required for osteoblast differentiation. …

Autoimmune Neuromuscular Disorders at a Molecular Crossroad: Linking Pathogenesis to Targeted Immunotherapy.

Myasthenia gravis, chronic inflammatory demyelinating polyneuropathy, and idiopathic inflammatory myopathies are among the most widely recognized autoimmune neuromuscular disorders. Although they differ in clinical presentation, shared immunopathogenic mechanisms place them at a molecular crossroads. Evidence of overlapping pathways has led to the development of targeted strategies including complement inhibition, FcRn antagonism, B-cell depletion, and the CAR-T cell approach. In this review, we analyze current knowledge regarding pathogenic mechanisms and their link to immunotherapy, extensiv

Cellular and molecular mechanisms of muscle atrophy.

Skeletal muscle is a plastic organ that is maintained by multiple pathways regulating cell and protein turnover. During muscle atrophy, proteolytic systems are activated, and contractile proteins and organelles are removed, resulting in the shrinkage of muscle fibers. Excessive loss of muscle mass is associated with poor prognosis in several diseases, including myopathies and muscular dystrophies, as well as in systemic disorders such as cancer, diabetes, sepsis and heart failure. Muscle loss also occurs during aging. In this paper, we review the key mechanisms that regulate the turnover of co

The Roles of EDA2R in Ageing and Disease.

Ageing is a complex biological process driven, in part, by inflammaging. Recent research identifies the ectodysplasin A2 receptor (EDA2R) as a key regulator of inflammaging and a novel biomarker of ageing, with its expression increasing with age across diverse tissues in humans and animal models. Elevated EDA2R gene expression is associated with accelerated ageing, cellular senescence, frailty, obesity, acne, radiation response and increased levels of inflammatory, renal, cardiac and vascular biomarkers. Similarly, elevated EDA2R protein levels, a critical component of the proteomic ageing clo

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… Utilising single‐cell RNA sequencing data from murine and human skeletal muscle, they confirmed that this age‐related upregulation of EDA2R occurs across multiple cell types, including myotubes and myogenic precursors such as satellite cells and myoblasts. … Next, functional experiments revealed that forced overexpression of Eda2r in murine myoblasts led to a marked induction of inflammatory mediators, including Cxcl5 and Il6 , closely resembling the transcriptional profile of aged muscle. …

Резюме 18th Неевромускульная научно-исследовательская конференция Соединенного Королевства 15th и 16th апрель 2025.

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… In vitro experiments were conducted to assess the effects of EGF and EFEMP1 on FAPs and myoblasts, including their impact on myotube size, fibrotic differentiation, and muscle strength. … In contrast, EGF promoted fibrotic differentiation in FAPs and induced the formation of smaller, proliferative myotubes in myoblasts, contributing to a fibrotic and dysfunctional muscle phenotype. …

The Crosstalk Between B Cells and the Skeletal System During Development, Aging, and in Pathological Conditions.

Purpose of reviewIn this review, we describe the interaction between B cells and bone during development, aging, and disease. RECENT FINDINGS: There is an increased interest in identifying the mechanisms of interaction between immune cells and the skeletal system. This knowledge is critical for understanding the pathology of autoimmune diseases and developing therapeutic interventions. Humoral immunity depends on B cells and their secreted immunoglobulin (antibodies). Earlier studies described B cell influence on the skeletal system, with a major focus on the role of plasma cells and secreted

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… Among these cells are developing B cells that originate from Hematopoietic Stem Cells (HSCs) and osteoblasts, myoblasts, chondroblasts, and adipocytes that develop from MSCs. In humans, hematopoiesis is initiated in the yolk sac at 18 days post-conceptional age (PCA). … The use of the advanced technology of spatial transcriptomics and single cell sequencing, and intravital imaging will certainly identify specific B cell populations and specific RNA and protein targets that are involved in the crosstalk between B cells and osteoblasts, osteoclasts, chondrocytes, myoblasts …

Advances in the research on myokine-driven regulation of bone metabolism.

The traditional view posits that bones and muscles interact primarily through mechanical coupling. However, recent studies have revealed that myokines, proteins secreted by skeletal muscle cells, play a crucial role in the regulation of bone metabolism. Myokines are widely involved in bone metabolism, influencing bone resorption and formation by interacting with factors related to bone cell secretion or influencing bone metabolic pathways. Here, we review the research progress on the myokine regulation of bone metabolism, discuss the mechanism of myokine regulation of bone metabolism, explore

Сокращенная специфическая реакция на патогенную Т ячейку с BCMA-Targeted T Cell-Enging Therapy to Multieloma.

ВВЕДЕНИЕ: Биогенное лечение антител (BsAb) может привести к увеличению числа инфекций у пациентов миэломы. Мы использовали ELISpot и цитометрию потока для проверки реакции T клеток на BCMA-CD3-диаграмму T-активиста (Bite) павурутамаб (PAV) и BCMA-выражающие клетки миэломы после внутривидовой культуры. Результаты: Снижение реакции на патогены было обнаружено в Т клетках, выращенных с PVV, но они уничтожили клетки миэломы. В исследовательском исследовании, в PBMC были обнаружены мягкие отзывы T-клеток, полученные от четырех пациентов миэломы, реагировавших на терапию BCMA. ЗАКЛЮЧЕНИЕ: Наше предв