Evidence map›Paper›PMID 41324784›Full record

ReviewMetabolic brain disease2025

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

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

Abstract readReview
PubMed Publisher
In one paragraph

Review in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Ahmed Salem Al-DhahiConsultant Neurology, Department of Neuroscience, King Fahad Specialist Hospital, Tabuk, Saudi Arabia.
Hayder M Al-KuraishyDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, P.O. Box 14132, Iraq.ORCID http://orcid.org/0000-0003-3097-2962
Ali I Al-GareebHead of Jabir ibn Hayyan Medical University, Al-Ameer Qu./Najaf, P.O.Box13, Kufa, Iraq.
Ali K AlbuhadilyDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, P.O. Box 14132, Iraq.
Aya M MustafaDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Egyptian Russian University, Badr City, Cairo, 11829, Egypt. aya-mustafa@eru.edu.eg.
Alaa IsmailSchool of Medicine, Taif University, Taif, Saudi Arabia.
Athanasios AlexiouUniversity Centre for Research & Development, Chandigarh University, Chandigarh-Ludhiana Highway, Mohali, Punjab, India.
Marios PapadakisDepartment of Surgery II, University Hospital Witten-Herdecke, University of Witten-Herdecke, Heusnerstrasse 40, 42283, Wuppertal, Germany. drmariospapadakis@gmail.com.
Gaber El-Saber BatihaDepartment of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, AlBeheira, 22511, Egypt. Gaberelsaberbatiha@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Diabetes Mellitus, Type 2Hypoglycemic AgentsMetforminMyasthenia GravisAMP-Activated Protein KinasesAnimalsHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesAMP-Activated Protein KinasesHypoglycemic AgentsMetforminMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesMetforminMyasthenia gravisPI3K/AKT/mTOR/AMPK signalingType 2 diabetes

Identifiers

PMID41324784

What Socratic holds

Texttitle and abstract
Read underepoch 390

Registered trials

None linked

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 Socratic graph.