ArticleBioMed research international2014
Local overexpression of V1a-vasopressin receptor enhances regeneration in tumor necrosis factor-induced muscle atrophy.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 246 citations in OpenAlex.
- Arginine-Vasopressin Dynamics in Relation to Food Intake and 8-Week Intranasal Oxytocin Treatment in Adults With Obesity.The Journal of clinical endocrinology and metabolism · 2025Trial
- Increased copeptin may reflect vasopressin-related metabolic changes after bariatric surgery.Obesity (Silver Spring, Md.) · 2025Article
- Taurine Administration Counteracts Aging-Associated Impingement of Skeletal Muscle Regeneration by Reducing Inflammation and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Article
- Neurohypophyseal hormones and skeletal muscle: a tale of two faces.European journal of translational myology · 2020Article
- Thyroid Hormone Protects from Fasting-Induced Skeletal Muscle Atrophy by Promoting Metabolic Adaptation.International journal of molecular sciences · 2019Article
- Oxytocin and Vasopressin Systems in Obesity and Metabolic Health: Mechanisms and Perspectives.Current obesity reports · 2019Review
- Inhibition of Phosphoinositide 3-Kinase/Protein Kinase B Signaling Hampers the Vasopressin-dependent Stimulation of Myogenic Differentiation.International journal of molecular sciences · 2019Article
- Skeletal Muscle: A Significant Novel Neurohypophyseal Hormone-Secreting Organ.Frontiers in physiology · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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Abstract
Skeletal muscle atrophy occurs during disuse and aging, or as a consequence of chronic diseases such as cancer and diabetes. It is characterized by progressive loss of muscle tissue due to hypotrophic changes, degeneration, and an inability of the regeneration machinery to replace damaged myofibers. Tumor necrosis factor (TNF) is a proinflammatory cytokine known to mediate muscle atrophy in many chronic diseases and to inhibit skeletal muscle regeneration. In this study, we investigated the role of Arg-vasopressin-(AVP-)dependent pathways in muscles in which atrophy was induced by local overexpression of TNF. AVP is a potent myogenesis-promoting factor and is able to enhance skeletal muscle regeneration by stimulating Ca(2+)/calmodulin-dependent kinase and calcineurin signaling. We performed morphological and molecular analyses and demonstrated that local over-expression of the AVP receptor V1a enhances regeneration of atrophic muscle. By upregulating the regeneration/differentiation markers, modulating the inflammatory response, and attenuating fibrogenesis, the stimulation of AVP-dependent pathways creates a favourable environment for efficient and sustained muscle regeneration and repair even in the presence of elevated levels of TNF. This study highlights a novel in vivo role for AVP-dependent pathways, which may represent an interesting strategy to counteract muscle decline in aging or in muscular pathologies.
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