ArticleSkeletal muscle2014
The injury-induced myokine insulin-like 6 is protective in experimental autoimmune myositis.
Article in Skeletal muscle, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Comprehensive analysis of interactions between brain aging and late-onset psychoses using heuristic mapping models.Communications medicine · 2026Article
- Qigu capsule alleviates dexamethasone-induced muscle dysfunction through mitochondrial biogenesis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- The diverse influences of relaxin-like peptide family on tumor progression: Potential opportunities and emerging challenges.Heliyon · 2024Review
- Single-cell transcriptomic analysis reveals rich pituitary-Immune interactions under systemic inflammation.PLoS biology · 2023Article
- Myocardial Infarction-Induced INSL6 Decrease Contributes to Breast Cancer Progression.Disease markers · 2023Article
- Major histocompatibility complex I-induced endoplasmic reticulum stress mediates the secretion of pro-inflammatory muscle-derived cytokines.Journal of cellular and molecular medicine · 2022Article
- Comparison of rapamycin and methylprednisolone for treating inflammatory muscle disease in a murine model of experimental autoimmune myositis.Experimental and therapeutic medicine · 2020Article
- Role of Myokines in Myositis Pathogenesis and Their Potential to be New Therapeutic Targets in Idiopathic Inflammatory Myopathies.Journal of immunology research · 2020Review
- Relaxin Family Member Insulin-Like Peptide 6 Ameliorates Cardiac Fibrosis and Prevents Cardiac Remodeling in Murine Heart Failure Models.Journal of the American Heart Association · 2018Article
- In vivo generation of a mature and functional artificial skeletal muscle.EMBO molecular medicine · 2015Article
- Development of an improved animal model of experimental autoimmune myositis.International journal of clinical and experimental pathology · 2015Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe idiopathic inflammatory myopathies represent a group of autoimmune diseases that are characterized by lymphocyte infiltration of muscle and muscle weakness. Insulin-like 6 (Insl6) is a poorly characterized member of the insulin-like/relaxin family of secreted proteins, whose expression is upregulated upon acute muscle injury.
methodsIn this study, we employed Insl6 gain or loss of function mice to investigate the role of Insl6 in a T cell-mediated model of experimental autoimmune myositis (EAM). EAM models in rodents have involved immunization with human myosin-binding protein C with complete Freund's adjuvant (CFA) emulsions and pertussis toxin.
resultsInsl6-deficiency in mice led to a worsened myositis phenotype including increased infiltration of CD4 and CD8 T cells and the elevated expression of inflammatory cytokines. Insl6-deficient mice show significant motor function impairment when tested with treadmill or Rotarod devices. Conversely, muscle-specific overexpression of Insl6 protected against the development of myositis as indicated by reduced lymphocyte infiltration in muscle, diminished inflammatory cytokine expression and improved motor function. The improvement in myositis by Insl6 could also be demonstrated by acute hydrodynamic delivery of a plasmid encoding murine Insl6. In cultured cells, Insl6 inhibits Jurkat cell proliferation and activation in response to phytohemagglutinin/phorbol 12-myristate 13-acetate stimulation. Insl6 transcript expression in muscle was reduced in a cohort of dermatomyositis and polymyositis patients.
conclusionsThese data suggest that Insl6 may have utility for the treatment of myositis, a condition for which few treatment options exist.
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