scholarly journals Unfolding the pathogenesis of systemic sclerosis through epigenomics

STEMedicine ◽  
2020 ◽  
Vol 1 (1) ◽  
pp. e5
Author(s):  
Xiuzhi Jia ◽  
Hao Cheng ◽  
Ying Xiao
Keyword(s):  
Dna Methylation ◽  
Systemic Sclerosis ◽  
Autoimmune Diseases ◽  
Environmental Stress ◽  
Histone Modification ◽  
Immune Dysregulation ◽  
Epigenetic Mechanisms ◽  
Internal Organs ◽  
Current Information ◽  
Epigenetic Alteration

As a group of autoimmune diseases, systemic sclerosis (scleroderma, SSc) is characterized by immune dysregulation, micro-vessels dominant obliteration, and the final fibrosis of the skin and or internal organs. Although the precise mechanisms are still unknown, increasing data shows that epigenetic mechanisms, such as DNA methylation, histone modification, and microRNA (miRNA), are strictly related to the pathogenesis of scleroderma. Epigenetic mechanisms, which can link genetics and environmental stress, represents a promising field in systemic sclerosis investigation. The objective of this review is, to sum up the current information about epigenetic alteration.

scholarly journals Epigenetics and Autoimmune Diseases

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Paula Quintero-Ronderos ◽  
Gladis Montoya-Ortiz
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Nucleotide Sequence ◽  
Autoimmune Diseases ◽  
Histone Modification ◽  
Disease Progression ◽  
Regulation Of Gene Expression ◽  
Epigenetic Mechanisms ◽  
Clinical Markers ◽  
Epigenetic Research

Epigenetics is defined as the study of all inheritable and potentially reversible changes in genome function that do not alter the nucleotide sequence within the DNA. Epigenetic mechanisms such as DNA methylation, histone modification, nucleosome positioning, and microRNAs (miRNAs) are essential to carry out key functions in the regulation of gene expression. Therefore, the epigenetic mechanisms are a window to understanding the possible mechanisms involved in the pathogenesis of complex diseases such as autoimmune diseases. It is noteworthy that autoimmune diseases do not have the same epidemiology, pathology, or symptoms but do have a common origin that can be explained by the sharing of immunogenetic mechanisms. Currently, epigenetic research is looking for disruption in one or more epigenetic mechanisms to provide new insights into autoimmune diseases. The identification of cell-specific targets of epigenetic deregulation will serve us as clinical markers for diagnosis, disease progression, and therapy approaches.

scholarly journals The Role of Sulforaphane in Epigenetic Mechanisms, Including Interdependence between Histone Modification and DNA Methylation

2015 ◽  
Vol 16 (12) ◽  
pp. 29732-29743 ◽  
Author(s):  
Agnieszka Kaufman-Szymczyk ◽  
Grzegorz Majewski ◽  
Katarzyna Lubecka-Pietruszewska ◽  
Krystyna Fabianowska-Majewska
Keyword(s):  
Dna Methylation ◽  
Histone Modification ◽  
Epigenetic Mechanisms

scholarly journals The Role of PPAR Gamma in Systemic Sclerosis

PPAR Research ◽  
2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Andréa Tavares Dantas ◽  
Michelly Cristiny Pereira ◽  
Moacyr Jesus Barreto de Melo Rego ◽  
Laurindo Ferreira da Rocha ◽  
Ivan da Rocha Pitta ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Lung Fibrosis ◽  
Ppar Gamma ◽  
Immune Dysregulation ◽  
Unknown Etiology ◽  
Internal Organs ◽  
Medical Need

Fibrosis is recognized as an important feature of many chronic diseases, such as systemic sclerosis (SSc), an autoimmune disease of unknown etiology, characterized by immune dysregulation and vascular injury, followed by progressive fibrosis affecting the skin and multiple internal organs. SSc has a poor prognosis because no therapy has been shown to reverse or arrest the progression of fibrosis, representing a major unmet medical need. Recently, antifibrotic effects of PPARγligands have been studiedin vitroandin vivoand some theories have emerged leading to new insights. Aberrant PPARγfunction seems to be implicated in pathological fibrosis in the skin and lungs. This antifibrotic effect is mainly related to the inhibition of TGF-β/Smad signal transduction but other pathways can be involved. This review focused on recent studies that identified PPARγas an important novel pathway with critical roles in regulating connective tissue homeostasis, with emphasis on skin and lung fibrosis and its role on systemic sclerosis.

Pathogenesis of systemic sclerosis: recent insights of molecular and cellular mechanisms and therapeutic opportunities

2017 ◽  
Vol 2 (3) ◽  
pp. 137-152 ◽  
Author(s):  
John Varga ◽  
Maria Trojanowska ◽  
Masataka Kuwana
Keyword(s):  
Systemic Sclerosis ◽  
Complex Disease ◽  
Repair Process ◽  
Immune Dysregulation ◽  
Lipid Mediators ◽  
Oxygen Species ◽  
Cellular Mechanisms ◽  
Internal Organs ◽  
Matrix Deposition ◽  
Pathogenic Process

Systemic sclerosis (SSc) is a complex disease characterized by early microvascular abnormalities, immune dysregulation and chronic inflammation, and subsequent fibrosis of the skin and internal organs. Excessive fibrosis, distinguishing hallmark of SSc, is the end result of a complex series of interlinked vascular injury and immune activation, and represents a maladaptive repair process. Activated vascular, epithelial, and immune cells generate pro-fibrotic cytokines, chemokines, growth factors, lipid mediators, autoantibodies, and reactive oxygen species. These paracrine and autocrine cues in turn induce activation, differentiation, and survival of mesenchymal cells, ensuing tissue fibrosis through increased collagen synthesis, matrix deposition, tissue rigidity and remodeling, and vascular rarefaction. This review features recent insights of the pathogenic process of SSc, highlighting three major characteristics of SSc, microvasculopathy, excessive fibrosis, and immune dysregulation, and sheds new light on the understanding of molecular and cellular mechanisms contributing to the pathogenesis of SSc and providing novel avenues for targeted therapies.

scholarly journals The Roles of Epigenetics Regulation in Bone Metabolism and Osteoporosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Fei Xu ◽  
Wenhui Li ◽  
Xiao Yang ◽  
Lixin Na ◽  
Linjun Chen ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Histone Modification ◽  
Osteogenic Differentiation ◽  
Bone Metabolism ◽  
Bone Fragility ◽  
Research Progress ◽  
Epigenetic Mechanisms ◽  
Mineral Density ◽  
Transcriptional Regulatory ◽  
Non Coding Rnas

Osteoporosis is a metabolic disease characterized by decreased bone mineral density and the destruction of bone microstructure, which can lead to increased bone fragility and risk of fracture. In recent years, with the deepening of the research on the pathological mechanism of osteoporosis, the research on epigenetics has made significant progress. Epigenetics refers to changes in gene expression levels that are not caused by changes in gene sequences, mainly including DNA methylation, histone modification, and non-coding RNAs (lncRNA, microRNA, and circRNA). Epigenetics play mainly a post-transcriptional regulatory role and have important functions in the biological signal regulatory network. Studies have shown that epigenetic mechanisms are closely related to osteogenic differentiation, osteogenesis, bone remodeling and other bone metabolism-related processes. Abnormal epigenetic regulation can lead to a series of bone metabolism-related diseases, such as osteoporosis. Considering the important role of epigenetic mechanisms in the regulation of bone metabolism, we mainly review the research progress on epigenetic mechanisms (DNA methylation, histone modification, and non-coding RNAs) in the osteogenic differentiation and the pathogenesis of osteoporosis to provide a new direction for the treatment of bone metabolism-related diseases.

scholarly journals Epigenetics and gestational diabetes: a review of epigenetic epidemiology studies and their use to explore epigenetic mediation and improve prediction

Diabetologia ◽  
2019 ◽  
Vol 62 (12) ◽  
pp. 2171-2178 ◽  
Author(s):  
Hannah R. Elliott ◽  
Gemma C. Sharp ◽  
Caroline L. Relton ◽  
Deborah A. Lawlor
Keyword(s):  
Type 2 Diabetes ◽  
Dna Methylation ◽  
Gestational Diabetes ◽  
Histone Modification ◽  
Diabetes Research ◽  
Epigenetic Mechanisms ◽  
Epigenetic Epidemiology ◽  
Epigenetic Biomarkers

Abstract Epigenetics encapsulates a group of molecular mechanisms including DNA methylation, histone modification and microRNAs (miRNAs). Gestational diabetes (GDM) increases the risk of adverse perinatal outcomes and is associated with future offspring risk of obesity and type 2 diabetes. It has been hypothesised that epigenetic mechanisms mediate an effect of GDM on offspring adiposity and type 2 diabetes and this could provide a modifiable mechanism to reduce type 2 diabetes in the next generation. Evidence for this hypothesis is lacking. Epigenetic epidemiology could also contribute to reducing type 2 diabetes by identifying biomarkers that accurately predict risk of GDM and its associated future adverse outcomes. We reviewed published human studies that explored associations between any of maternal GDM, type 2 diabetes, gestational fasting or post-load glucose and any epigenetic marker (DNA methylation, histone modification or miRNA). Of the 81 relevant studies we identified, most focused on the potential role of epigenetic mechanisms in mediating intrauterine effects of GDM on offspring outcomes. Studies were small (median total number of participants 58; median number of GDM cases 27) and most did not attempt replication. The most common epigenetic measure analysed was DNA methylation. Most studies that aimed to explore epigenetic mediation examined associations of in utero exposure to GDM with offspring cord or infant blood/placenta DNA methylation. Exploration of any causal effect, or effect on downstream offspring outcomes, was lacking. There is a need for more robust methods to explore the role of epigenetic mechanisms as possible mediators of effects of exposure to GDM on future risk of obesity and type 2 diabetes. Research to identify epigenetic biomarkers to improve identification of women at risk of GDM and its associated adverse (maternal and offspring) outcomes is currently rare but could contribute to future tools for accurate risk stratification.

scholarly journals Contribution of Dysregulated DNA Methylation to Autoimmunity

2021 ◽  
Vol 22 (21) ◽  
pp. 11892
Author(s):  
Samanta C. Funes ◽  
Ayleen Fernández-Fierro ◽  
Diego Rebolledo-Zelada ◽  
Juan P. Mackern-Oberti ◽  
Alexis M. Kalergis
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Epigenetic Modifications ◽  
Epigenetic Mechanisms ◽  
Epigenetic Alterations ◽  
Development And Differentiation ◽  
Differential Gene ◽  
The Impact

Epigenetic mechanisms, such as DNA methylation, histone modifications, and non-coding RNAs are known regulators of gene expression and genomic stability in cell growth, development, and differentiation. Because epigenetic mechanisms can regulate several immune system elements, epigenetic alterations have been found in several autoimmune diseases. The purpose of this review is to discuss the epigenetic modifications, mainly DNA methylation, involved in autoimmune diseases in which T cells play a significant role. For example, Rheumatoid Arthritis and Systemic Lupus Erythematosus display differential gene methylation, mostly hypomethylated 5′-C-phosphate-G-3′ (CpG) sites that may associate with disease activity. However, a clear association between DNA methylation, gene expression, and disease pathogenesis must be demonstrated. A better understanding of the impact of epigenetic modifications on the onset of autoimmunity will contribute to the design of novel therapeutic approaches for these diseases.

scholarly journals The Function of the Metals in Regulating Epigenetics During Parkinson’s Disease

2021 ◽  
Vol 11 ◽  
Author(s):  
Xiangzhen Wei ◽  
Menghua Cai ◽  
Lifang Jin
Keyword(s):  
Parkinson’S Disease ◽  
Dna Methylation ◽  
Central Nervous System ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Histone Modification ◽  
Motor System ◽  
Epigenetic Mechanism ◽  
Epigenetic Mechanisms ◽  
Global Hypomethylation

Parkinson’s means Parkinson’s disease, a chronic degenerative disease of central nervous system. The main area which is affected by this disease is motor system. Since it firstly founded by James Parkinson in his 1817 publication, nowadays, people still have lots of questions about this disease. This review mainly summarizes the epigenetics of Parkinson’s. DNA methylation is one of the epigenetic mechanisms of Parkinson’s. During the development of disease, global hypomethylation, and hypermethylation happen in different areas of patients. Another epigenetic mechanism is histone modification. People believe that some metals can induce Parkinson’s disease by modulating epigenetic mechanisms. This review summarizes the relationships between different metals and Parkinson’s disease. However, the specific roles of most metals in epigenetics are still unknown, which need further research.

scholarly journals The Involvement of Metals in Alzheimer’s Disease Through Epigenetic Mechanisms

2020 ◽  
Vol 11 ◽  
Author(s):  
Menghua Cai ◽  
Xiangjin Zhang ◽  
Wei He ◽  
Jianmin Zhang
Keyword(s):  
Heavy Metals ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dna Methylation ◽  
Histone Modification ◽  
Epigenetic Mechanisms ◽  
Genes And Environment ◽  
Two Factors ◽  
Environment Factor ◽  
Amyloid Cascade

Alzheimer’s disease (AD) is the most frequent cause of dementia among neurodegenerative diseases. Two factors were hypothesized to be involved in the pathogenesis of AD, namely beta-amyloid cascade and tauopathy. At present, accumulating evidence suggest that epigenetics may be the missing linkage between genes and environment factors, providing possible clues to understand the etiology of the development of AD. In this article, we focus on DNA methylation and histone modification involved in AD and the environment factor of heavy metals’ contribution to AD, especially epigenetic mechanisms. If we can integrate information together, and that may find new potential targets for the treatment.

scholarly journals Epigenetic Mechanisms Underlying Adult Post Stroke Neurogenesis

2020 ◽  
Vol 21 (17) ◽  
pp. 6179
Author(s):  
Xianshuang Liu ◽  
Baoyan Fan ◽  
Michael Chopp ◽  
Zhenggang Zhang
Keyword(s):  
Dna Methylation ◽  
Stem Cell ◽  
Histone Modification ◽  
Cell Fate ◽  
Epigenetic Mechanisms ◽  
Cell Fate Determination ◽  
Epigenetic Factors ◽  
Self Renewal ◽  
Post Stroke ◽  
Non Coding Rnas

Stroke remains the leading cause of adult disability. Post-stroke neurogenesis contributes to functional recovery. As an intrinsic neurorestorative process, it is important to elucidate the molecular mechanism underlying stroke-induced neurogenesis and to develop therapies designed specifically to augment neurogenesis. Epigenetic mechanisms include DNA methylation, histone modification and its mediation by microRNAs and long-non-coding RNAs. In this review, we highlight how epigenetic factors including DNA methylation, histone modification, microRNAs and long-non-coding RNAs mediate stroke-induced neurogenesis including neural stem cell self-renewal and cell fate determination. We also summarize therapies targeting these mechanisms in the treatment of stroke.

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