ArticleJournal of neuroinflammation2025
Hypothalamic kisspeptin alleviates myasthenia gravis by regulating Th1/Th17/Treg balance through Inhibition of NF-κB signaling pathway.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Naringenin protects against renal ischemia-reperfusion injury following unilateral nephrectomy via modulation of oxidative stress and kisspeptin expression.International urology and nephrology · 2026Article
- The role and mechanism of IL‑35 in myasthenia gravis (Review).International journal of molecular medicine · 2026Review
- Quercetin as a multifaceted neuroprotective agent against cerebral ischaemia-reperfusion injury: mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- Cytokine Changes With Effective Drug Therapy for Juvenile Myasthenia Gravis.Journal of immunology research · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundMyasthenia gravis (MG) is an autoimmune disorder affecting neuromuscular junctions. While neuroendocrine-immune system dysfunction plays a crucial role in the development of autoimmune diseases, its involvement in MG remains largely unexplored. Kisspeptin, a neuropeptide hormone and endogenous ligand for GPR54 receptor, has been demonstrated to regulate antitumor immunity, antiviral immunity, and several autoimmune diseases. However, the role and mechanism of kisspeptin in MG remain to be elucidated.
methodsSerum kisspeptin levels were measured by ELISA in MG patients and experimental autoimmune myasthenia gravis (EAMG) rats. EAMG rats were treated with KP10 (kisspeptin analog) to evaluate its effects on body weight, clinical scores, grip strength, antibody levels, and complement deposition. Hypothalamic Kiss1 expression was assessed using Western blot and immunofluorescence. Stereotactic injection of adeno-associated virus overexpressing Kiss1 was performed to study its regulatory effects on disease progression. CD4
resultsKisspeptin expression was significantly decreased in both MG patient sera and EAMG rat sera, with reduced hypothalamic Kiss1 expression in EAMG rats. Either hypothalamic Kiss1 overexpression or intraperitoneal KP10 administration significantly improved clinical signs in EAMG rats. Further in vivo and in vitro studies revealed that KP10 ameliorated EAMG clinical signs by modulating Th1/Th17/Treg cell balance through inhibition of NF-κB signaling pathway activation in CD4
conclusionThis study elucidates that Kisspeptin secreted by hypothalamic participates in MG pathogenesis through the Kisspeptin-GPR54-NF-κB signaling axis by regulating CD4
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