Epigenetic involvement in etiopathogenesis and implications in treatment of systemic lupus erythematous

Foma, Arron Munggela; Aslani, Saeed; Karami, Jafar; Jamshidi, Ahmadreza; Mahmoudi, Mahdi

doi:10.1007/s00011-017-1082-y

Cited by 24 publications

(12 citation statements)

References 141 publications

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“…Therefore, they are implicated in the formation of cell‐ and tissue‐specific phenotypes. Although the epigenetic modifications are highly stable, they can be modified by environmental factors and thereby act as a vital mechanism for cell survival and adaptation to the new condition or disease . Epigenetic mechanisms are theoretically involved in three important aspects of RA: contribution to disease etiology, involvement in the mechanisms of the disease development, and act as robust biomarkers of disease progression and activity .…”

Section: Involvement Of Epigenetics In Ra Pathogenesismentioning

confidence: 99%

“…Although the epigenetic modifications are highly stable, they can be modified by environmental factors and thereby act as a vital mechanism for cell survival and adaptation to the new condition or disease. 15,16 Epigenetic mechanisms are theoretically involved in three important aspects of RA: contribution to disease etiology, involvement in the mechanisms of the disease development, and act as robust biomarkers of disease progression and activity. 17 Surprisingly, studies on monozygotic and dizygotic twins have showed that the role of epigenetics is more significant than that of genetics with regard to RA susceptibility.…”

Section: Involvement Of Epigenetics In Ra Pathogenesismentioning

confidence: 99%

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Epigenetics in rheumatoid arthritis; fibroblast‐like synoviocytes as an emerging paradigm in the pathogenesis of the disease

et al. 2020

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Rheumatoid arthritis (RA) is characterized by immune dysfunctions and chronic inflammation that mainly affects diarthrodial joints. Genetics has long been surveyed in searching for the etiopathogenesis of the disease and partially clarified the conundrums within this context. Epigenetic alterations, such as DNA methylation, histone modifications, and noncoding RNAs, which have been considered to be involved in RA pathogenesis, likely explain the nongenetic risk factors. Epigenetic modifications may influence RA through fibroblast‐like synoviocytes (FLSs). It has been shown that FLSs play an essential role in the onset and exacerbation of RA, and therefore, they may illustrate some aspects of RA pathogenesis. These cells exhibit a unique DNA methylation profile in the early stage of the disease that changes with disease progression. Histone acetylation profile in RA FLSs is disrupted through the imbalance of histone acetyltransferases and histone deacetylase activity. Furthermore, dysregulation of microRNAs (miRNAs) is immense. Most of these miRNAs have shown an aberrant expression in FLSs that are involved in proliferation and cytokine production. Besides, dysregulation of long noncoding RNAs in FLSs has been revealed and attributed to RA pathogenesis. Further investigations are needed to get a better view of epigenetic alterations and their interactions. We also discuss the role of these epigenetic alterations in RA pathogenesis and their therapeutic potential.

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Section: Involvement Of Epigenetics In Ra Pathogenesismentioning

confidence: 99%

Section: Involvement Of Epigenetics In Ra Pathogenesismentioning

confidence: 99%

Epigenetics in rheumatoid arthritis; fibroblast‐like synoviocytes as an emerging paradigm in the pathogenesis of the disease

et al. 2020

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“…DNA methylation involves in many cellular phenomena such as X-chromosome inactivation, transposable retro element activities, cell differentiation, cell reprogramming, cell death, cell survival, parental gene imprinting, immune system activities and allelic exclusion of immunoglobulin genes [12,13]. DNA methylation abnormalities are linked with different diseases such as cancer, autoimmune diseases and atherosclerosis [14][15][16][17][18][19]. Investigations on DNA methylation in patients with atherosclerosis documented that there is a unique profile of DNA methylation in this disease, and emphasize on the different pathways and genes which are implicated in the disease [20].…”

Section: Introductionmentioning

confidence: 99%

DNA methylation abnormalities in atherosclerosis

Tabaei

Tabaee

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Atherosclerosis is a complex disease with involvement of intermediate-, large-sized arteries. Atherosclerosis is characterized by the accumulation of vascular lipids, immune system activation, inflammation, oxidative stress and oxidized low-density lipoproteins (LDLs), endothelial cell (EC) activation, arterial smooth muscle cell (SMC) proliferation, macrophage activation and foam cell formation that cause endothelial dysfunction. DNA methylation is one of important epigenetic mechanisms which changes gene expression. It has been evident that this mechanism plays an important role in the initiation and propagation of atherosclerosis. Furthermore, DNA methylation is a crucial and distinct mechanism that modulates genes governing cell proliferation, thereby connecting environmental insults with gene expression. This study represents many atherosclerosis-related genes which are regulated through DNA methylation mechanism. Although the role of epigenetics in atherosclerosis is at their infancy. Nevertheless, various studies demonstrated that DNA methylation involvement in this disease is undeniable. DNA methyltransferases are the main player of the smooth muscle cell proliferation, endothelial cell integrity, as well as arteriosclerosis formation. In this review, we focus on recent achievements in the functional and description interpretation of the DNA methylation pattern of cells and tissues implicated in atherosclerosis. Besides, we discuss the association of DNA methylation with oxidative stress, hyperhomocysteinemia (HHcy), ageing, and inflammation in the development and pathogenesis of atherosclerosis.

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“…There are several issues which need to be addressed. In case of DNA methylation, it is not completely clear that DNA methylation abnormalities, which are reported through different studies [25,[33][34][35][36][37], are actually consequence of the disease or could be considered as a disease causes. Since the DNA methylation could be affected by disease stage and chronic inflammatory situation of disease, it seems that these abnormalities are a disease consequence rather than the disease cause.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of CX3CR1 gene DNA methylation in developmental dysplasia of the hip (DDH)

et al. 2022

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Introduction and objective Developmental dysplasia of the hip (DDH) is a musculoskeletal disorder. Genetic and epigenetic changes in C-X3-C motif chemokine receptor 1 (CX3CR1) may lead to disturbance in chondrocyte development and change the labrum dimensions, which indirectly result in hip joint instability. Considering the important role of this gene in cell migration, cell adhesion and bone and cartilage development, we aimed to evaluate the CX3CR1 gene methylation in DDH pathogenesis. Methods Our study comprised of forty-five DDH patients and forty-five healthy control subjects with healthy femoral neck cartilage. The healthy controls had total or hemiarthroplasty for the femoral neck fracture. Samples were collected from the femoral head (cartilage) of DDH patients and healthy controls. Genomic DNA was obtained from the samples, and DNA methylation of CX3CR1 gene was analyzed via metabisulfite method. Results Methylation analysis reveals no significant differences in promoter of CX3CR1 gene in cartilage samples from DDH patients and healthy control subjects (P = 0.33). Conclusion Methylation status of CX3CR1 gene showed no significant difference between the patient and control groups. Our results indicate that DNA methylation may not modulate this gene in this disease and other epigenetic mechanisms such as non-coding RNAs and histone modifications could be implicated.

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Epigenetic involvement in etiopathogenesis and implications in treatment of systemic lupus erythematous

Abstract: Accumulating evidence disclosed that epigenetic dysregulations are engaged in SLE pathogenesis and may be exerted as biomarkers to diagnose and as tools to treat these patients.

Cited by 24 publications

References 141 publications

Epigenetics in rheumatoid arthritis; fibroblast‐like synoviocytes as an emerging paradigm in the pathogenesis of the disease

Epigenetics in rheumatoid arthritis; fibroblast‐like synoviocytes as an emerging paradigm in the pathogenesis of the disease

DNA methylation abnormalities in atherosclerosis

Evaluation of CX3CR1 gene DNA methylation in developmental dysplasia of the hip (DDH)

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