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Feb 2022 DOI 10.14302/issn.2379-8572.joa-22-4072
This translational paper discusses differentiation‑stage factors from zebrafish embryos as epigenetic regulators with potential to reverse neurosensory hearing loss. It outlines experimental evidence, delivery concepts, and research gaps.
Aug 2019 DOI 10.14302/issn.2572-3030.jcgb-19-2973
Head and Neck cancer (HNC) is one of the most prevalent and lethal cancer globally. The incidence of tobacco-induced HNC is gradually increasing in low and middle income countries. Among the various causative factors associated with HNCs, tobacco and alcohol play synergistic effect and are frequently associated with the risk of HNC. Tobacco-induced HNCs show distinct genetic and epigenetic alterations leading to different clinical outcomes in comparison to HPV-infected HNCs. Tobacco-induced HNCs are often associated with tumor aggressiveness, poor prognosis and low or nil prevalence of HPV infection. Apart from carcinogenic effects of these causative factors (use of tobacco products, alcohol intake and HPV or EBV infections), recent studies show that exposure to these factors alter/disrupt the regulation of non-coding RNAs including the long non-coding RNAs (lncRNAs). Altered lncRNA regulation is brought about by signalling networks that regulate cellular differentiation, apoptosis, angiogenesis and inflammatory pathways which play key functions in the genesis of different cancers including HNCs. There are numbers of studies supporting the emerging role of lncRNAs in development of HNC; however, reports connecting lncRNAs expression and addiction habits in HNC are still preliminary and sparse. Therefore, identification and characterization of lncRNAs that are differentially expressed upon exposure to risk-factors can serve as unique therapeutic targets and potential biomarker(s) for effective treatment of HNC subtypes. In this short review, we briefly reviewed the emerging role of lncRNAs in tobacco and alcohol induced HNCs.
Jun 2019 DOI 10.14302/issn.2688-5328.ijp-19-2731
The rise of epigenetics provides a new idea for studying the regulation of chronic pain-related genes and synaptic plasticity. External environmental stimuli can regulate BDNF genes through different epigenetic modifications. The epigenetic changes of the BDNF gene can affect the expression of its mRNA and protein and participate in the development of chronic pain. By reviewing the literature, this paper reviews the mechanism of epigenetic regulation of brain-derived neurotrophic factor (BDNF) in chronic pain, which provides some new directions and targets for the treatment of chronic pain.
Nov 2018 DOI 10.14302/issn.2572-3030.jcgb-18-2428
Head and neck cancers (HNCs) are the most prevalent and aggressive type of cancers. Genetic, epigenetic, environmental and viral risk-factors are associated with HNC carcinogenesis. Persistent infection of oncogenic human papillomaviruses (HR-HPVs) represent distinct biological, molecular and epigenetic entities in HNCs. There are three main epigenetic mechanisms that regulate transcription, these are DNA methylation, histone modifications and alteration in non-coding RNA networks, which can dissected to identify innovative and accurate epigenetic biomarkers for diagnosis and prognosis of HNC patients. Due to the lacunae of accurate distinctive biomarkers for the definite diagnosis of HNC, the identification of predictive epigenetic markers is necessary that might modify or increase HNC patient’s survival. In this mini review, we briefly summarize the current knowledge of different epigenetic biomarkers in HNC.
Sep 2018 DOI 10.14302/issn.2641-9467.jgrc-18-2270
Rice, as one of the most important crops in the world, is facing an ever-accelerating challenge from climate change. Epigenetic modification with its substantially high epimutation rate and the possibility for some epigenetic variation to act as a heritable contributor to crop environmental adaptability may hold great potentials for rapid crop breeding. Epigenetic modification is controlled by epigenetic pathways, and mutations disturbing the epigenetic pathways may lead to significant epigenetic and/or genetic changes. This is especially true for rice, whose genome is rich in epigenetic modifications and transposable elements (TEs) that are generally epigenetically silenced. Here, in this paper, we first reviewed the pathways that establish, maintain and remove rice DNA methylation, which is the most well studied epigenetic marker, as well as the genes that are involved. We then discussed how TEs amplify the phenotypic impact of epigenetic changes that could be a result of epigenetic pathway disturbances. At last, we presented the enormous amount of rice genome data that are publically available, within which great genetic variation in the genes that are involved within the epigenetic pathways is embedded. This genetic variation awaits to be exploited for their potentials in generating a heritable source of variation for rapid environmental adaptation, which may hold tremendous importance for rice breeding in the face of climate change.
May 2018
Genetics alone cannot thoroughly expound the environmental impact on the molecular complexity of the endocrine system. Epigenetic-induced alteration in gene expression has emerged as a way in which environmental compounds may exert endocrine effects. The environmental compounds that interfere with normal endocrine signaling are one of the largest classes of toxicants we are exposed to, on a daily basis. Epigenetic mechanisms, mainly the methylation of DNA and the modification of histones, lead to differentiated activation and deactivation of genome domains creating phenotype plasticity and divergent endocrine function among populations and individuals, as well. The issues examined in the present review are related to environmental epigenetics, and more precisely, the epigenetic-mediated modulation and relevance of endocrine disrupting chemicals, focusing on three broad aspects: 1) persistence of EDs, 2) their major hormonal effects and 3) the potential of compounds previously considered as endocrine disruptors to induce epigenetic effects. Evidence suggests that environmental exposures notably impact expression of endocrine-related genes and, thus, affect clinical endocrine outcomes.
May 2015 DOI 10.14302/issn.2379-7835.ijn-14-603
Epigenetic mechanisms based on DNA methylation, histone modifications and RNA interference have recently showed important association to the development of a wide variety of diseases such as cancer, cardiovascular, metabolic, skin, autoimmune diseases and neurologic disorders. In the context of preventive aspects, the importance of nutrition on epigenetic function has been revealed. Therefore, drastic changes in dietary modifications may contribute to reduced disease risk. For instance, dietary intervention has been showed to affect DNA methylation in Alzheimer’s disease patients. Moreover, maternal high-fat diet can regulate gene expression through promoter histone modifications. Most importantly, RNA interference and particularly micro-RNA mediated regulation of gene expression has been linked to disease development. Remarkably, dietary intake has been demonstrated to significantly affect various miRNAs and their regulation on gene function. In this review, the relationship between epigenetics and disease and development of drugs based on epigenetic targets is presented as well as the influence of dietary intake on epigenetic mechanisms and its effect on disease prevention and therapy will be discussed.
Nov 2025 DOI 10.14302/issn.3070-5657.je-24-5327
Human embryonic development is a highly coordinated and complex process that transforms a single fertilized cell into a fully formed human organism. This process is governed by intricate molecular mechanisms involving genetic regulation, signal transduction pathways, and intercellular communication. This study explores key molecular pathways controlling human embryonic development, focusing on the roles of morphogens, transcription factors, signaling molecules, and epigenetic modifications. By reviewing the most recent literature and experimental studies, we aim to highlight the molecular orchestration that directs cell fate decisions, tissue patterning, and organogenesis in humans.
Mar 2021 DOI 10.14302/issn.2329-9487.jhc-21-3742
Cardiovascular disease is actually a major cause of mortality, illness and hospitalization worldwide. Several risk factors have been identified that are strongly associated with the development of cardiovascular disease. Public prevention strategies have relied predominately on managing environmental factors that contribute to cardiovascular disease, such as obesity, smoking and lack of exercise. The understanding of the role of genetics in cardiovascular disease development has become much more important to link genetics with the onset of disease and response to therapy. This seeks to examine how genes can predispose individuals to cardiovascular disease and how this knowledge might be applied to more comprehensive preventive strategies in the future. In addition, the review explores possibilities for genetics in cardiovascular disease treatment, particularly through the use of identified driver genes and gene therapy. To fully understand the biological implications of these associations, there is a need to relate them to the exquisite, multilayered regulation of protein expression and regulatory elements, mutation, microRNAs and epigenetics. Understanding how the information contained in the DNA relates to the operation of these regulatory layers will allow us not only to better predict the development of cardiovascular disease but also to develop more effective therapies.
Aug 2018 DOI 10.14302/issn.2689-4602.jes-18-2229
A historical and conceptual review traces how evolutionary theory has expanded from classical selection to modern syntheses incorporating development, epigenetics, and systems thinking. Implications for research and science communication are discussed.
Jun 2018 DOI 10.14302/issn.2689-4602.jes-18-2128
Natural selection is a buzzword used to describe the main driving force of evolution. Its creative role is believed to be based on: a) an unlimited variety of organisms caused by hereditary variation and b) a direct connection between hereditary changes and their phenotypic expression. These are the two requirements that can lead to the genetically based changing modalities of characters through “iterations” of natural selection in the series of successive generations. Are these two requirements fulfilled in the nature, however? The present study focuses on the analysis of these two “foundation stones” of natural selection. Firstly, hereditary variation is shown to be essentially non-homogenous. New hereditary characteristics of individuals fall onto a narrow “strip of land” in the sea of potential possibilities. Secondly, the consequences of changes in the genotype of an organism are involved into a system of hierarchical multiple compensation, from the molecular to the biocenotic level. In a way, the signal of hereditary change passes through a series of “system filters” at epigenetic, ontogenetic, physiological, behavioural, populational and biocenotic level. Each filter is represented by multiple feedbacks maintaining the integrity of systems at each level and at all the hierarchical levels taken together. It is in these “system filters” the adaptive nature of characters is formed representing the every individual as a subject to the Law of Multilevel Self-Organization. The emerging understanding of this provides a strong reason to change the evolutionary paradigm from the mainly selectogenetic to the mainly orthogenetic one.
Aug 2017 DOI 10.14302/issn.2572-3030.jcgb-14-383
Meningiomas are the most common intracranial tumor in humans. The heterogeneity of these tumors lends difficulty to the genetic, epigenetic, and molecular changes that occur in meningioma pathogenesis, progression, and recurrence. Current de facto classification schemes are based on histologic evaluation of tumor specimens and do not consider molecular markers or other newer modalities. In this paper, we review the major genetic, epigenetic, and molecular changes that have been associated with the oncogenesis and progression of meningiomas. We pay special attention to those changes associated with recurrence and higher grade tumors. Finally, we comment on the challenges and potential for future therapies of these tumors.
Sep 2013 DOI 10.14302/issn.2374-9431.jbd-13-226
The number of individuals with diabetes is increasing worldwide and a large subset of those affected will develop diabetic nephropathy. Diabetic nephropathy is the leading cause of end-stage renal disease, has serious health consequences for affected individuals, and represents a major monetary cost to healthcare providers. Technological and analytical developments have enabled large-scale, collaborative studies that are revealing risk factors associated with diabetic nephropathy. However, much of the inherited predisposition and biological mechanisms underpinning risk of this disease remain to be identified. Meta-analyses and integrated pathway studies are becoming an increasingly important part of research for diabetic nephropathy including, genetic, epigenetic, transcriptomic, proteomic research, clinical observations and the development of animal models. This report highlights current bioinformatic resources and standards of reporting to maximise interdisciplinary research for diabetic nephropathy. The identification of an -Omics profile that can lead to earlier diagnosis and / or offer improved clinical evaluation of individuals with diabetes would not only provide significant health benefits to affected individuals, but may also have major utility for the efficient use of healthcare resources.