Regulation of the cellular redox state and the expression of DNA methyltransferase-1 in peripheral blood mononuclear cells from patients with Graves’ disease

Saban, Melina; Costilla, Melisa; Klecha, Alicia Juana; Cugno, Mariana Di; Curriá, Marina; Cremaschi, Graciela; Arcos, Marı́a Laura Barreiro

doi:10.1016/j.endinu.2021.07.011

Cited by 1 publication

(1 citation statement)

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“…LncRNA may also sponge miRNA and regulate DNA transcription, with relevance in rheumatoid arthritis [31]; (iii) DNA methyltransferase (DNMT) and ten eleven translocation (TET) modulate gene transcription via the hypermethylation and hypomethylation of cytosine in DNA, respectively. DNMT-1 is proposed to regulate immune responses, as shown in Graves' disease [32], whilst Tet methylcytosine dioxygenase 2 (Tet2) deficiency drives hepatic microbiome dysbiosis, leading to CD8 + T cell-mediated autoimmune hepatitis [33]; (iv) N 6 -methyladenosine (m 6 A) is a common modification of both mRNA and DNA, whereby the METTL3/METTL14 methyltransferase complex installs m 6 A onto mRNA, which can impact not only translation, but also nuclear export and decay, as well as pre-mRNA processing, with relevance to immune regulation in T1DM [34].…”

Section: Classical Autoimmunitymentioning

confidence: 99%

Redefining Autoimmune Disorders’ Pathoetiology: Implications for Mood and Psychotic Disorders’ Association with Neurodegenerative and Classical Autoimmune Disorders

Anderson¹,

Almulla

Reíter

et al. 2023

Cells

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Although previously restricted to a limited number of medical conditions, there is a growing appreciation that ‘autoimmune’ (or immune-mediated) processes are important aspects of a wide array of diverse medical conditions, including cancers, neurodegenerative diseases and psychiatric disorders. All of these classes of medical conditions are associated with alterations in mitochondrial function across an array of diverse cell types. Accumulating data indicate the presence of the mitochondrial melatonergic pathway in possibly all body cells, with important consequences for pathways crucial in driving CD8+ T cell and B-cell ‘autoimmune’-linked processes. Melatonin suppression coupled with the upregulation of oxidative stress suppress PTEN-induced kinase 1 (PINK1)/parkin-driven mitophagy, raising the levels of the major histocompatibility complex (MHC)-1, which underpins the chemoattraction of CD8+ T cells and the activation of antibody-producing B-cells. Many factors and processes closely associated with autoimmunity, including gut microbiome/permeability, circadian rhythms, aging, the aryl hydrocarbon receptor, brain-derived neurotrophic factor (BDNF) and its receptor tyrosine receptor kinase B (TrkB) all interact with the mitochondrial melatonergic pathway. A number of future research directions and novel treatment implications are indicated for this wide collection of poorly conceptualized and treated medical presentations. It is proposed that the etiology of many ‘autoimmune’/‘immune-mediated’ disorders should be conceptualized as significantly determined by mitochondrial dysregulation, with alterations in the mitochondrial melatonergic pathway being an important aspect of these pathoetiologies.

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