MicroRNAs and Diabetes Mellitus Type 1

Bahreini, Farbod; Rayzan, Elham; Rezaei, Nima

doi:10.2174/1573399817666210215111201

Cited by 6 publications

(3 citation statements)

References 89 publications

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“…Furthermore, histone modifications have shown their influence on immune response gene dysregulation in the context of T1D (72). The role of microRNAs, another facet of epigenetics, has also been underscored, particularly in controlling immune and inflammatory responses in T1D (61,(73)(74)(75)(76). Epigenetic alterations associated with T1D risk not only hold implications for biomarker discovery but also open doors to precision medicine strategies in T1D diagnosis, risk assessment, and therapeutic intervention.…”

Section: Gene-environment Interaction and T1dmentioning

confidence: 99%

Gene-environment interaction in the pathophysiology of type 1 diabetes

Mittal,

Camick,

Lemos

et al. 2024

Front. Endocrinol.

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Type 1 diabetes (T1D) is a complex metabolic autoimmune disorder that affects millions of individuals worldwide and often leads to significant comorbidities. However, the precise trigger of autoimmunity and disease onset remain incompletely elucidated. This integrative perspective article synthesizes the cumulative role of gene-environment interaction in the pathophysiology of T1D. Genetics plays a significant role in T1D susceptibility, particularly at the major histocompatibility complex (MHC) locus and cathepsin H (CTSH) locus. In addition to genetics, environmental factors such as viral infections, pesticide exposure, and changes in the gut microbiome have been associated with the development of T1D. Alterations in the gut microbiome impact mucosal integrity and immune tolerance, increasing gut permeability through molecular mimicry and modulation of the gut immune system, thereby increasing the risk of T1D potentially through the induction of autoimmunity. HLA class II haplotypes with known effects on T1D incidence may directly correlate to changes in the gut microbiome, but precisely how the genes influence changes in the gut microbiome, and how these changes provoke T1D, requires further investigations. These gene-environment interactions are hypothesized to increase susceptibility to T1D through epigenetic changes such as DNA methylation and histone modification, which in turn modify gene expression. There is a need to determine the efficacy of new interventions that target these epigenetic modifications such as “epidrugs”, which will provide novel avenues for the effective management of T1D leading to improved quality of life of affected individuals and their families/caregivers.

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Section: Gene-environment Interaction and T1dmentioning

confidence: 99%

Gene-environment interaction in the pathophysiology of type 1 diabetes

Mittal,

Camick,

Lemos

et al. 2024

Front. Endocrinol.

View full text Add to dashboard Cite

show abstract

“…Diabetes mellitus type 1 [89] Anti-insulin, anti-IA-2, anti-GAD, anti-ZnT8 antibodies Discoid lupus erythematosus [90] ANA, Anti-dsDNA, Anti-Sm Eosinophilic granulomatosis with polyangiitis (EGPA) [91] Anti-streptolysin O (ASO), anti-DNase B Epidermolysis bullosa acquisita [92] Anti-type VII collagen…”

Section: Disease Autoantibodymentioning

confidence: 99%

Anti-Idiotypic mRNA Vaccine to Treat Autoimmune Disorders

Niazi

2023

Vaccines

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The 80+ existing autoimmune disorders (ADs) affect billions with little prevention or treatment options, except for temporary symptomatic management, leading to enormous human suffering and a monumental financial burden. The autoantibodies formed in most ADs have been identified, allowing the development of novel anti-idiotypic antibodies to mute the autoantibodies using vaccines. Nucleoside vaccines have been successfully tested as antigen-specific immunotherapies (ASI), with mRNA technology offering multi-epitope targeting to mute multiple autoantibodies. This paper proposes using mRNA technology to produce anti-idiotypic antibodies with broad effectiveness in preventing and treating them. This paper delves into the state-of-the-art mRNA design strategies used to develop novel ASIs by selecting appropriate T cell and B cell epitopes to generate anti-idiotypic antibodies. The low cost and fast development of mRNA vaccines make this technology the most affordable for the global control of ADs.

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“…[13,14] microRNAs (miRNAs) are small noncoding RNAs, which are involved in many physiological and pathological processes, and their role in type 1 diabetes as an autoimmune disease is welldocumented. [15] miRNAs enhance or inhibit inflammation under pathological conditions. miRNAs bind to TLRs and regulate TLRmediated inflammatory responses through different mechanisms.…”

mentioning

confidence: 99%

Tropisetron improved testicular inflammation in the streptozotocin‐induced diabetic rats: The role of toll‐like receptor 4 (TLR4) and mir146a

Naderi

Pourheydar

Moslehi

2022

J Biochem & Molecular Tox

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As a serotonin antagonist, tropisetron positively affects blood glucose lowering, insulin synthesis, pancreas inflammation, and apoptosis in diabetes. Reproductive disorders are one of the diabetes‐induced chronic complications. The present study aimed to evaluate the effect of tropisetron on diabetes‐induced testicular inflammation, its signaling pathway, and mir146a. To this end, animals were assigned to the control, tropisetron, diabetes (DM), DM‐tropisetron, and DM‐glibenclamide groups. Streptozotocin (50 mg/kg) was intraperitoneally injected to provide diabetes. Tropisetron and glibenclamide were then administrated intraperitoneally for 2 weeks after diabetes induction. Testes histology, real‐time polymerase chain reaction, western blot analysis, ELISA, and immunohistochemistry assays were also performed. The finding revealed that tropisetron significantly improved diabetes‐induced testis damages, lowered TLR4, TRAF6, IRAK1, NF‐κB, and caspase3 protein expressions, and decreased TNF‐α and IL‐1 levels. Moreover, the mir146a expression declined following the tropisetron treatment. This study demonstrated that the significant role of tropisetron in lowering testicular inflammation and apoptosis might have been due to the inhibition of the TLR4/IRAK1/TRAF6 signaling pathway and thereby the attenuation of NF‐κB and caspase3 expression and inflammatory cytokines. Furthermore, the downregulation of mir146a, as an inflammatory microRNA interacting with TLR4, showed another pathway, through which tropisetron improved diabetes‐induced testicular injuries.

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MicroRNAs and Diabetes Mellitus Type 1

Cited by 6 publications

References 89 publications

Gene-environment interaction in the pathophysiology of type 1 diabetes

Gene-environment interaction in the pathophysiology of type 1 diabetes

Anti-Idiotypic mRNA Vaccine to Treat Autoimmune Disorders

Tropisetron improved testicular inflammation in the streptozotocin‐induced diabetic rats: The role of toll‐like receptor 4 (TLR4) and mir146a

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