ArticleMolecular therapy. Nucleic acids2018
Hepatocyte Growth Factor Regulates the miR-206-HDAC4 Cascade to Control Neurogenic Muscle Atrophy following Surgical Denervation in Mice.
Article in Molecular therapy. Nucleic acids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- An open-label single-arm phase 1/2a study to evaluate the safety and exploratory efficacy of a VM202 in patients with Charcot-Marie-Tooth disease 1A.Orphanet journal of rare diseases · 2026Trial
- The miR-206-3p/Cpeb1 axis delays acetylcholine receptor degradation and preserves neuromuscular junction stability in denervation-induced muscle atrophy.Cellular and molecular life sciences : CMLS · 2026Article
- Hereditary Polyneuropathies in the Era of Precision Medicine: Genetic Complexity and Emerging Strategies.Genes · 2026Review
- Article
- Epigenetics in the formation of pathological aggregates in amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2024Review
- Novel rAAV vector mediated intrathecal HGF delivery has an impact on neuroimmune modulation in the ALS motor cortex with TDP-43 pathology.Gene therapy · 2023Article
- Construction of Plasmid DNA Expressing Two Isoforms of Insulin-Like Growth Factor-1 and Its Effects on Skeletal Muscle Injury Models.Human gene therapy · 2022Article
- TIMP-1-expressing breast tumor spheroids for the evaluation of drug penetration and efficacy.Bioengineering & translational medicine · 2022Article
- Lack ofeLife · 2022Article
- CUL3 and COPS5 Related to the Ubiquitin-Proteasome Pathway Are Potential Genes for Muscle Atrophy in Mice.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- FGF2-primed 3D spheroids producing IL-8 promote therapeutic angiogenesis in murine hindlimb ischemia.NPJ Regenerative medicine · 2021Article
- The role of physical activity and miRNAs in the vascular aging and cardiac health of dialysis patients.Physiological reports · 2021Article
- Protective effects of acute exercise preconditioning on disuse-induced muscular atrophy in aged muscle: a narrative literature review.The journal of physiological sciences : JPS · 2020Review
- MicroRNA-206 Regulates Stress-Provoked Aggressive Behaviors in Post-weaning Social Isolation Mice.Molecular therapy. Nucleic acids · 2020Article
- Hepatocyte Growth Factor Regulates Macrophage Transition to the M2 Phenotype and Promotes Murine Skeletal Muscle Regeneration.Frontiers in physiology · 2019Article
- Microarray Analysis of Gene Expression Provides New Insights Into Denervation-Induced Skeletal Muscle Atrophy.Frontiers in physiology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocyte growth factor (HGF) has been well characterized for its roles in the migration of muscle progenitors during embryogenesis and the differentiation of muscle stem cells, but its function in adult neurogenic muscle atrophic conditions is poorly understood. Here we investigated whether HGF/c-met signaling has any effects on muscle-atrophic conditions. It was found that HGF expression was upregulated in skeletal muscle tissue following surgical denervation and in hSOD1-G93A transgenic mice showing severe muscle loss. Pharmacological inhibition of the c-met receptor decreased the expression level of pri-miR-206, enhanced that of HDAC4 and atrogenes, and resulted in increased muscle atrophy. In C2C12 cells, HGF inhibited phosphorylation of Smad3 and relieved TGF-β-mediated suppression of miR-206 expression via JNK. When extra HGF was exogenously provided through intramuscular injection of plasmid DNA expressing HGF, the extent of muscle atrophy was reduced, and the levels of all affected biochemical markers were changed accordingly, including those of primary and mature miR-206, HDAC4, and various atrogenes. Taken together, our finding suggested that HGF might play an important role in regard to neurogenic muscle atrophy and that HGF might be used as a platform to develop therapeutic agents for neuromuscular disorders.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.