MyMiR (HC2101) / Zhejiang Haichang Biotech - LARVOL DELTA

Integrated analysis of MYH6, MYH7, and MYH7B expression and their associated microRNAs in human end-stage heart failure. (PubMed, Front Cardiovasc Med) - "We further observed a dissociation between miR-208a-3p and its host gene (MYH6) under physiological conditions and confirmed altered miR-499a-5p/MYH7B relationships, consistent with findings in murine models. Moreover, the expression of two regulatory genes, SOX6 and TARBP2, known to modulate MYH7 and MYH7B in mice, showed that SOX6 is upregulated in the left ventricles of all pathological groups."

Journal • Cardiomyopathy • Cardiovascular • Congestive Heart Failure • Coronary Artery Disease • Heart Failure • Hypertrophic Cardiomyopathy • MIR208A • MIR499A • MYH7

Tiny Molecules, Mighty Impacts: MicroRNAs in Neuromuscular Diseases (ICNMD 2026) - "This review aimed to demonstrate current knowledge on the role of myomiRs in major NMDs, particullary Duchenne muscular dystrophy (DMD), myotonic dystrophy type 1 (DM1), limb-girdle muscular dystrophy (LGMD), McArdle disease, and myofibrillar myopathy (MFM), emphasizing their biological significance and clinical potential. A narrative literature review was conducted using indexed databases to identify studies addressing myomiR expression, function, and clinical implications in neuromuscular diseases. The analysis demonstrated that specific myomiRs, such as miR-1, miR-133a/b, miR-206, miR-29b, miR-31, and miR-486, are differentially expressed among these disorders, participating in processes like muscle degeneration, regeneration, fibrosis, and inflammation... MyomiRs are central to the molecular mechanisms of NMDs and stand out as accessible biomarkers for diagnosis, monitoring, and therapeutic evaluation. Their emerging use as non-invasive endpoints in clinical trials..."

CNS Disorders • Duchenne Muscular Dystrophy • Fibrosis • Genetic Disorders • Immunology • Inflammation • Muscular Dystrophy • Myositis • Myotonic Dystrophy • MIR143 • MIR206 • MIR223 • MIR31 • MIR486-1

Skeletal muscle‑derived extracellular vesicles in multi‑organ degenerative disease: Mechanisms and therapeutic delivery perspectives (Review). (PubMed, Int J Mol Med) - "The present review examines the biological functions of SkM‑EVs, their regulation by exercise, aging and metabolic stress and their potential involvement in multi‑organ degenerative diseases. The present study aimed to discuss engineering strategies for SkM‑EVs, including cargo loading, surface modification and targeted delivery, with particular attention to controversies, methodological limitations, quality control requirements and barriers to clinical translation."

Journal • Review • Cardiovascular • Chronic Kidney Disease • CNS Disorders • Congestive Heart Failure • Diabetes • Heart Failure • Immunology • Metabolic Disorders • Nephrology • Osteoarthritis • Osteoporosis • Pain • Renal Disease • Rheumatology • Sarcopenia

Molecular Mechanisms of MyomiR-133b–Mediated Tumor Suppression in HCT116 Colorectal Cancer Cells (EACR 2026) - "These findings indicate that myomiR-133b suppresses colorectal cancer proliferation through YAP downregulation, resulting in reduced Survivin expression, p27/Kip1 stabilization, and cell-cycle arrest. Simultaneous induction of TAZ and survival-related signalling proteins points to a compensatory adaptive response."

Colorectal Cancer • Oncology • Solid Tumor • AFP • AXL • BIRC5 • EGFR • MIR133B • SKP2

MyomiR Networks in Spinal Muscular Atrophy: Associations With Clinical Severity and Treatment Response. (PubMed, Mol Neurobiol) - "Using RT-qPCR, we assessed associations between baseline RNA expression and demographic and clinical parameters, including SMA type, ambulatory status, motor and respiratory function, and explored longitudinal changes during nusinersen (24 months) and risdiplam (6/12 months) treatment. In contrast, risdiplam induced a peripheral splicing shift: SMN-FL and the FL/∆7 ratio increased, while SMN-∆7 decreased; miR-133a-3p also decreased at 6 months. By integrating muscle-derived RNAs, particularly miR-206, with blood SMN2 splicing changes, we propose a composite, blood-based biomarker approach for assessing SMA status and treatment-associated molecular changes and highlight myomiR-lncRNA-mRNA networks that suggest disease-relevant mechanisms."

Journal • Genetic Disorders • Movement Disorders • Muscular Atrophy • Rare Diseases • ANXA2 • FGFR1 • GJA1 • MIR133B • MIR206 • SMN2

Omic technology to monitoring resilience and adaptation to exercise and heat stress in endurance horses. (PubMed, Front Vet Sci) - "Differentially expressed small RNAs included eca-myomir-206, eca-mir-301, eca-mir-3613-3p, eca-mir-142, and eca-mir-144, which were modulated by temperature and exercise...Overall, our findings indicate that heat amplifies the physiological burden of endurance exercise and alters the molecular mechanisms supporting performance and recovery. Circulating small RNAs may act as early signals for homeostatic restoration and could help elucidate adaptive responses to stress, guiding personalized training strategies."

Journal • Cardiovascular • CNS Disorders • Inflammation • Vascular Neurology • MIR142 • MIR144 • MIR206 • MIR301A • MIR3613

The Mutation of myomiR miR499 Impacts the Intermuscular Bones in Zebrafish. (PubMed, Biology (Basel)) - "Our findings establish miR499 as a key regulator of a muscle-bone functional axis, where miRNA-mediated muscle fiber specification determines mechanical output that subsequently guides IB development. This work provides new insights into the mechanobiological regulation of skeletal development and identifies a promising genetic target for aquaculture breeding programs aimed at attenuated IBs."

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Strength training and sarcopenia-a mandatory link: focus on MicroRNAs. (PubMed, Front Aging) - "Some of them are expressed differently by subjects affected by sarcopenia (as happens in various forms of cancer or other diseases). Therefore, monitoring a specific signature of microRNAs can better clarify the etiopathology of sarcopenia, providing an early biomarker for sarcopenia (currently, there are some hypotheses, but none is well recognized), and even serve as the basis for the development of drugs."

Journal • Review • Oncology • Sarcopenia

MyomiR-133b suppresses colorectal cancer cell proliferation and modulates expression of multiple gene targets (EACR 2025) - "This study provides evidence that myomiR-133b suppresses CRC proliferation, which may be mediated through the regulation of transcription factors (SRF), deacetylases (Sirtuin1, HDAC4) and genes related to cancer cell proliferation and apoptosis (P53, LIF). The mechanisms of tumour-suppressing effect of exercise-conditioned human plasma will require further research. Grant support: VEGA-2/0144/23, Sedlárová-Rabanová scholarship, APVV 19-0411, APVV 23-0604"

Colorectal Cancer • Genetic Disorders • Obesity • Oncology • Solid Tumor • HDAC4 • MIR133B • SIRT1 • TIMP1

microRNA-133a as an indicator of disease progression and treatment response in X-linked myotubular myopathy. (PubMed, Mol Ther Nucleic Acids) - "miR-133a is a muscle-enriched non-coding RNA (myomiR) involved in muscle development and function and is implicated in the regulation of the XLMTM modifier gene DNM2...Moreover, we show that miR-133a expression in treated Mtm1 KO mice positively correlates with treatment response and was shown to have high discrimination accuracy for XLMTM by linear discriminant analysis (79%-90%) and receiver operating characteristic curve analysis (AUC >0.80). These results support miR-133a as a robust, circulating biomarker that reflects disease severity and treatment response in XLMTM."

Journal • CNS Disorders • Myositis • Pediatrics

Muscle-specific miRNAs in plasma and skeletal muscle of patients with idiopathic inflammatory myopathy are modulated by disease and training. (PubMed, Rheumatology (Oxford)) - "Lower myomiR levels in skeletal muscle of IIM patients might indicate reduced muscle regenerative potential in IIM, which could be linked to inflammation, metabolic dysfunction, and immunosuppressive therapy. Training-induced changes of muscle and plasma myomiRs indicate an increase in myomiRs release, which could contribute to the adaptive response underlying the positive systemic effects of exercise in IIM."

Journal • Inflammation • Metabolic Disorders • Myositis • MIR133B • MIR206

Extracellular vesicle miR-206 improves chronic binge alcohol mediated decreased myoblast differentiation in SIV-infected female macaques. (PubMed, Am J Physiol Cell Physiol) - "Myotube and myotube derived EV myomiR expression, including miR-206, was lower in the CBA/SIV group...Similarly, EV-mediated delivery of miR-206 increased both fusion index and myotube density of CBA/SIV-derived myoblasts. These results support the potential therapeutic utility of EVs in delivering myomiRs to improve SKM stem cell differentiation."

Journal • Human Immunodeficiency Virus • Infectious Disease • HDAC4 • MIR206 • PAX7

Increased Expression of MiRNA-1 Contributes to Hypobaric Hypoxia-Induced Skeletal Muscle Loss. (PubMed, Adv Biol (Weinh)) - "Studies found the potential role of miR-1 (myomiR) as a biomarker under different atrophic conditions...This study indicates the increased expressions of miR-1 and reduced expression of PAX3 and HSP70 lead to impaired myogenesis in skeletal muscle under HH. Further, enhanced expression of muscle degradation genes such as FOXO3, MSTN, and ATROGIN under HH exposure causes skeletal muscle protein loss."

Journal • Muscular Atrophy • FOXO3 • PAX3

EV-mediated promotion of myogenic differentiation is dependent on dose, collection medium, and isolation method. (PubMed, Mol Ther Nucleic Acids) - "Furthermore, we observed pro-myogenic effects with undifferentiated myoblast-derived EVs, in which myomiR concentrations are even lower, suggestive of a myomiR-independent mechanism underlying the observed pro-myogenic effects...Specifically, co-purification of insulin (a component of Opti-MEM) in non-EV LC fractions and polymer precipitated EV preparations. These findings provide further evidence that polymer-based precipitation techniques should be avoided in EV research."

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