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<p>Myasthenia gravis (MG) represents the commonest autoimmune disorder affecting the neuromuscular junction (NMJ). The pathophysiology of MG is mainly linked to the formation of IgG autoantibodies directed against acetylcholine receptors (AChRs) in the NMJ. Besides, type 2 diabetes (T2D) is observed as a conceivable risk factor for the development and progression of MG. Also, T2D is further related with late-onset MG than early-onset MG. Nevertheless, there are no differences in the levels of autoantibodies in T2D patients with MG compared to T2D patients without MG. It has been proposed that increasing the production of advanced glycation end-products (AGEs) proteins and the expression of receptor glycation end-products (RAGE) in early T2D provokes the autoimmunity in MG. Additionally; AGE/RAGE signaling is augmented and contributes in the progression of autoimmunity in MG. Nonetheless, the fundamental association between MG and T2D is not totally elucidated. Therefore, this review aims to discuss and explain the link between T2D and MG. Findings of the present review highlighted that metformin mitigates the pathogenesis of both T2D and MG by regulating of PI3K/AKT/mTOR/AMPK axis and enhancing autophagy.</p>

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Interconnection between myasthenia gravis and type 2 diabetes: emerging role of metformin in modulating PI3K/AKT/mTOR/AMPK axis

  • 期刊论文

  • 发表日期：

    2025年12月1日

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  • Ahmed salem Al-Dhahi,
  • Hayder M. Al-Kuraishy,
  • Ali I. Al-Gareeb,
  • Ali K. Albuhadily,
  • Aya M. Mustafa,
  • Alaa Ismail,
  • Athanasios Alexiou,
  • Marios Papadakis,
  • Gaber El-Saber Batiha

摘要

Myasthenia gravis (MG) represents the commonest autoimmune disorder affecting the neuromuscular junction (NMJ). The pathophysiology of MG is mainly linked to the formation of IgG autoantibodies directed against acetylcholine receptors (AChRs) in the NMJ. Besides, type 2 diabetes (T2D) is observed as a conceivable risk factor for the development and progression of MG. Also, T2D is further related with late-onset MG than early-onset MG. Nevertheless, there are no differences in the levels of autoantibodies in T2D patients with MG compared to T2D patients without MG. It has been proposed that increasing the production of advanced glycation end-products (AGEs) proteins and the expression of receptor glycation end-products (RAGE) in early T2D provokes the autoimmunity in MG. Additionally; AGE/RAGE signaling is augmented and contributes in the progression of autoimmunity in MG. Nonetheless, the fundamental association between MG and T2D is not totally elucidated. Therefore, this review aims to discuss and explain the link between T2D and MG. Findings of the present review highlighted that metformin mitigates the pathogenesis of both T2D and MG by regulating of PI3K/AKT/mTOR/AMPK axis and enhancing autophagy.