Although cancer cell gene expression profiles show diversity, the epigenetic mechanisms governing pluripotency-associated genes in prostate cancer have been studied more recently. Epigenetic mechanisms governing NANOG and SOX2 gene activity are central to this chapter's investigation of their influence in human prostate cancer, highlighting the specific actions of these transcription factors.
The epigenome encompasses all epigenetic alterations, including DNA methylation, histone modifications, and non-coding RNAs, which collectively influence gene expression and play a significant role in diseases such as cancer and other biological processes. Gene expression is under the control of epigenetic modifications, which influence variable gene activity at various levels and affect diverse cellular phenomena, including cell differentiation, variability, morphogenesis, and the adaptability of an organism. The epigenome is affected by numerous agents, ranging from dietary elements and environmental contaminants to the use of pharmaceutical products and the experience of stress. Epigenetic mechanisms are largely comprised of histone modifications, including post-translational alterations, and DNA methylation. Diverse strategies have been undertaken to scrutinize these epigenetic indicators. A commonly employed technique, chromatin immunoprecipitation (ChIP), enables the study of histone modifications and the binding of histone modifier proteins. Diverse variations of the ChIP technique exist, including reverse chromatin immunoprecipitation (R-ChIP), sequential ChIP (also known as ChIP-re-ChIP), and high-throughput adaptations like ChIP-seq and ChIP-on-chip. Methylation of the fifth carbon of cytosine within the DNA molecule is catalyzed by DNA methyltransferases (DNMTs), representing another epigenetic mechanism. Bisulfite sequencing, the oldest, and generally the most employed approach, assesses DNA methylation. Established methods for studying the methylome comprise whole-genome bisulfite sequencing (WGBS), methylated DNA immunoprecipitation (MeDIP), methylation-sensitive restriction enzyme sequencing (MRE-seq), and methylation BeadChips. Epigenetics in health and disease conditions is discussed in this chapter using key principles and the related methods.
Pregnancy-related alcohol abuse is a critical public health, economic, and social challenge, significantly affecting developing offspring. Human alcohol (ethanol) abuse during pregnancy is notably marked by neurobehavioral problems in the developing offspring, stemming from central nervous system (CNS) damage. This leads to both structural and behavioral issues collectively categorized as fetal alcohol spectrum disorder (FASD). To reproduce the characteristics of human Fetal Alcohol Spectrum Disorder (FASD), alcohol exposure models specific to developmental stages were designed to reveal the underlying mechanisms. The neurobehavioral problems following prenatal ethanol exposure may be explained, at a molecular and cellular level, by the findings from these animal studies. Although the underlying cause of Fetal Alcohol Spectrum Disorder (FASD) is yet to be definitively established, growing evidence indicates that varied genomic and epigenetic factors impacting gene expression levels could be major contributors to the development of this condition. These research endeavors identified diverse immediate and enduring epigenetic alterations, such as DNA methylation, post-translational histone protein modifications, and RNA-mediated regulatory networks, employing a variety of molecular techniques. Gene expression controlled by RNA, along with methylated DNA patterns and histone protein modifications, are critical for the development of synaptic and cognitive functions. Coelenterazine In this way, this furnishes a resolution to the numerous neuronal and behavioral issues often linked with FASD. The current chapter comprehensively analyzes recent progress in epigenetic modifications implicated in FASD etiology. The presented information has the potential to deepen our comprehension of FASD's origins, thereby providing a foundation for the development of novel therapeutic targets and innovative treatment methods.
The progressive decline in physical and mental capabilities, a hallmark of aging, ultimately culminates in increased vulnerability to illness and, inevitably, death, making it one of the most intricate and irreversible health conditions. These conditions demand attention from all, however, evidence indicates that physical activity, a nutritious diet, and beneficial routines can significantly mitigate the effects of aging. Numerous investigations have shown that epigenetics, notably DNA methylation, histone modifications, and non-coding RNA (ncRNA), substantially contribute to the aging process and associated diseases. human‐mediated hybridization Careful comprehension and appropriate adjustments to these epigenetic modifications may open up new possibilities for therapies aimed at delaying aging. Gene transcription, DNA replication, and DNA repair are impacted by these procedures, with epigenetics playing a central part in understanding aging and exploring potential pathways to slow aging, leading to clinical breakthroughs in mitigating age-related diseases and restoring vitality. This article details and champions the epigenetic contribution to aging and related illnesses.
Despite identical environmental exposures, monozygotic twins show varying upward trends in metabolic disorders like diabetes and obesity, prompting a consideration of the influence of epigenetic elements, including DNA methylation. The presented chapter summarizes emerging scientific evidence illustrating a strong correlation between DNA methylation modifications and the advancement of these diseases. Changes in the expression levels of diabetes/obesity-related genes, potentially due to methylation-mediated silencing, could be the root cause of this phenomenon. Genes displaying aberrant methylation are promising biomarkers for early disease prediction and diagnosis. In parallel, a study of methylation-based molecular targets is necessary for the development of new treatments for both type 2 diabetes and obesity.
The World Health Organization (WHO) has declared the rise of obesity a significant factor in the overall burden of disease and death. A negative spiral of effects emanates from obesity: impairing individual health, reducing quality of life, and generating long-term economic repercussions for the entire country. Histone modifications in the context of fat metabolism and obesity have become a subject of intensive study in recent years. Processes of epigenetic regulation are diverse and include methylation, histone modification, chromatin remodeling, and the modulation of microRNA expression. Cell development and differentiation are significantly impacted by these processes, primarily through gene regulation. This chapter investigates the characteristics of histone modifications in adipose tissue, exploring their diversity under diverse conditions, their contribution to adipose tissue development, and their correlation with biosynthesis processes in the body. The chapter, in addition, provides a comprehensive examination of histone modifications in obesity, the correlation between histone modifications and food consumption patterns, and the impact of histone modifications on overweight and obesity conditions.
The concept of an epigenetic landscape, introduced by Conrad Waddington, furnishes a metaphor for cell differentiation, depicting the progression from undifferentiated states to a spectrum of specialized cell fates. Epigenetic understanding has evolved dynamically, placing DNA methylation under the strongest research lens, followed by histone modifications and subsequently non-coding RNA. The prevalence of cardiovascular diseases (CVDs) has risen dramatically across the globe over the last two decades, making them a leading cause of death. A considerable allocation of resources is dedicated to examining the crucial mechanisms and underlying principles of various CVDs. By investigating genetics, epigenetics, and transcriptomics, these molecular studies aimed to uncover the mechanisms behind various cardiovascular conditions. The evolution of therapeutics has led to the development of epi-drugs, a crucial step in treating cardiovascular diseases over the past few years. Epigenetics' varied contributions to cardiovascular health and disease are the central focus of this chapter. A detailed examination of advancements in basic experimental techniques for epigenetics research, the role of epigenetics in cardiovascular diseases (including hypertension, atrial fibrillation, atherosclerosis, and heart failure), and emerging epi-therapeutic strategies will be undertaken, offering a comprehensive perspective on current collaborative efforts to advance epigenetic research in cardiovascular disease.
The most substantial research of the 21st century explores the dynamic relationship between human DNA sequences and the phenomenon of epigenetics. Inheritance biology and gene expression are influenced by a complex interplay between epigenetic shifts and environmental factors, both within and across generations. Various diseases' mechanisms have been shown by recent epigenetic studies to be explicable through the lens of epigenetics. To examine how epigenetic elements interact with varying disease pathways, the design and development of multidisciplinary therapeutic strategies was undertaken. We summarize in this chapter the ways in which an organism can be prone to specific diseases due to environmental exposures, such as chemicals, medications, stress, or infections, during vulnerable periods of life, and how the epigenetic component could affect some human diseases.
The social determinants of health (SDOH) encompass the circumstances in which people are born, the environments in which they live, and the conditions under which they work. Pulmonary pathology SDOH presents a more inclusive viewpoint on the critical role of environment, geographic location, neighborhood characteristics, healthcare availability, nutrition, socioeconomics, and various other aspects in affecting cardiovascular morbidity and mortality. The rising significance of SDOH in patient care management will inevitably lead to broader integration into clinical and healthcare systems, establishing the use of this information as commonplace.