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In 1878 evolutionary theoretician Edward D. Cope published an eight-page paper filled with prescient ideas that clearly anticipated theoretical evolutionary topics that are actively being debated some 145 years later. An examination of these ideas and their modern counterparts is the primary objective of this essay. A proposal is also made to provide an answer to Cope's Puzzle concerning the sequences of events involved in the evolution of adaptive animal structures. This article revisits Cope's "The Relation of Animal Motion to Animal Evolution" (published in The American Naturalist, volume 12, number 1, January 1878, pp. 40–48) for Biological Theory's "Classics in Biological Theory" collection; Cope's original paper is available as supplementary material in the online version of this article. [ABSTRACT FROM AUTHOR]

This paper is interested in normative translations of findings in intergenerational epigenetics. Particularly, what role can and should epigenetic knowledge play in our normative thinking about parenthood and relationships such as those between individual parents and broader society or between parents and their children? How should epigeneticists engage in science communication to ensure that knowledge of intergenerational epigenetic effects is useful rather than harmful to parents and children? Much of the existing literature on the ethical aspects of epigenetics points out worrisome tendencies of epigenetic knowledge inspiring policies and discourses that lead to blaming and stigmatization of individual parents and women in particular. While such warnings are important, they are not the only shape ethical discussion of intergenerational epigenetics can take. Firstly, this paper claims that it is also worthwhile and necessary to imagine potential positive effects of epigenetic knowledge on parents and their children. It will be argued that an approach that focuses on empowerment of individual parents and children rather than general responsibility distributions fits will with a nonideal approach to normative theory that takes into account the unequal distributions of social, economic and material resources among parents. The second part of this paper explores whether narrative identity is a useful concept to imagine such a positive framework for the employment of epigenetic knowledge. It argues that integration of epigenetic knowledge in a shared narrative identity may benefit mutual understanding and self-knowledge, and perhaps also have an empowering effect on parents, children and families. After discussing the risks of (1) attaching too much weight to etiology and (2) any epigenetics discourse playing into 'bionormativity', the paper concludes that epigenetic knowledge can and should be used in a framework that goes beyond deterministic etiologies but embraces the complexities and interrelatedness of all factors influencing the health of future generations. [ABSTRACT FROM AUTHOR]

This paper explores the significant role of epigenetics in women's reproductive health, focusing on the impact of environmental factors. It highlights the crucial link between epigenetic modifications--such as DNA methylation and histones post-translational modifications--and reproductive health issues, including infertility and pregnancy complications. The paper reviews the influence of pollutants like PM2.5, heavy metals, and endocrine disruptors on gene expression through epigenetic mechanisms, emphasizing the need for understanding how dietary, lifestyle choices, and exposure to chemicals affect gene expression and reproductive health. Future research directions include deeper investigation into epigenetics in female reproductive health and leveraging gene editing to mitigate epigenetic changes for improving IVF success rates and managing reproductive disorders. [ABSTRACT FROM AUTHOR]

Major depressive disorder (MDD) is a severe psychiatric illness known to be highly complex due to its difficulty in identifying genetic factors and its polygenic nature. While genetic studies and research into epigenetic changes have advanced our understanding of MDD, the precise role of genetics in MDD's manifestation remains elusive. This paper reviews the current state of research on MDD genetics, encompassing findings on MDD's biological blueprint and investigations into epigenetic modifications associated with MDD development. Furthermore, this paper explores the interplay between depression and the immune system and the impact of inflammation on the disorder. Neuroimaging studies have also impacted comprehension of MDD, revealing alterations in brain size and chemistry. These insights shed light on the biological underpinnings of MDD and hold promise for developing more effective treatments and therapies for patients. [ABSTRACT FROM AUTHOR]

Medulloblastoma (MB) is a highly malignant childhood brain tumor. Group 3 MB (Gr3 MB) is considered to have the most metastatic potential, and tailored therapies for Gr3 MB are currently lacking. Gr3 MB is driven by PRUNE-1 amplification or overexpression. In this paper, we found that PRUNE-1 was transcriptionally regulated by lysine demethylase LSD1/KDM1A. This study aimed to investigate the therapeutic potential of inhibiting both PRUNE-1 and LSD1/KDM1A with the selective inhibitors AA7.1 and SP-2577, respectively. We found that the pharmacological inhibition had a substantial efficacy on targeting the metastatic axis driven by PRUNE-1 (PRUNE-1-OTX2-TGFβ-PTEN) in Gr3 MB. Using RNA seq transcriptomic feature data in Gr3 MB primary cells, we provide evidence that the combination of AA7.1 and SP-2577 positively affects neuronal commitment, confirmed by glial fibrillary acidic protein (GFAP)-positive differentiation and the inhibition of the cytotoxic components of the tumor microenvironment and the epithelial–mesenchymal transition (EMT) by the down-regulation of N-Cadherin protein expression. We also identified an impairing action on the mitochondrial metabolism and, consequently, oxidative phosphorylation, thus depriving tumors cells of an important source of energy. Furthermore, by overlapping the genomic mutational signatures through WES sequence analyses with RNA seq transcriptomic feature data, we propose in this paper that the combination of these two small molecules can be used in a second-line treatment in advanced therapeutics against Gr3 MB. Our study demonstrates that the usage of PRUNE-1 and LSD1/KDM1A inhibitors in combination represents a novel therapeutic approach for these highly aggressive metastatic MB tumors. [ABSTRACT FROM AUTHOR]

Colorectal cancer is a malignant tumor with high morbidity and mortality worldwide. Histone lactylation, a new protein post-translational modification, can be used as a potential biomarker for the diagnosis and treatment of colorectal cancer by regulating the structure of chromatin and gene transcription. This paper focuses on the role and mechanism of histone lactylation modification in the development of colorectal cancer. Additionally, the latest research progress and clinical experimental results are presented. This paper further shows that histone lactylation manipulates gene expression by affecting nuclear transcription factors and other epigenetic modifications involved in various life processes and subsequently regulates cell physiological function, revealing its regulatory mechanism and the functions of related enzymes. The relationships between histone lactylation and energy metabolic pathways such as glycolysis and oxidative phosphorylation are discussed in detail. The final part of this paper illustrates the important role of this modification in terms of the occurrence and development of colorectal cancer, cell metabolic reprogramming, and epigenetic regulation, supporting the clinical application of the use of histone lactylation as a biomarker. [ABSTRACT FROM AUTHOR]

The Society for Molecular Biology and Evolution (SMBE) is celebrating the 40th anniversary of the first issue of Molecular Biology and Evolution by publishing a series of virtual issues in 2024. These virtual issues feature selected papers from the society's journals, Molecular Biology and Evolution and Genome Biology and Evolution. Each virtual issue is accompanied by a Perspective article that highlights the historical and contemporary contributions of the journals to a specific topic in molecular evolution. The September Perspective, titled "Epigenetics Research in Evolutionary Biology: Perspectives on Timescales and Mechanisms," was written by Soojin Yi and can be found in Molecular Biology and Evolution. The virtual issues include notable papers on Epigenetics and Evolution and can be accessed on SMBE's 40th anniversary site. [Extracted from the article]

Gastric cancer (GC) remains a significant public health concern because of its lethality, underscoring the need for deeper insights into its molecular mechanisms. Recent studies have increasingly highlighted the role of epigenetic modifications as critical players in cancer progression. Despite their importance, research specifically addressing epigenetic factors in GC is relatively scarce. This paper seeks to bridge that gap by examining recent literature that elucidates the epigenetic landscape associated with GC. The investigation of long noncoding RNAs (lncRNAs) has revealed their substantial involvement in gene dysregulation and epigenetic alterations within GC tumors. Notably, lncRNAs such as LINC00853 and LINC01266 have been identified as significant contributors to the epigenetic modulation of gene expression. Furthermore, the overexpression of KAT5 and GPX4 has been shown to mitigate the antiproliferative effects resulting from the depletion of circRHOT1, suggesting a complex interplay between these molecules in GC pathophysiology. Another pivotal aspect of epigenetic regulation in GC involves modifications in N6-methyladenosine (m6A), which play crucial roles in mRNA maturation processes such as splicing, export, degradation, and translation. m6A modifications are known for their influence on various cancer-related pathways, thus presenting a potential avenue for targeted interventions. Our findings indicate that the most pronounced instances of epigenetic dysregulation in GC can be traced back to the effects of long lncRNAs and alterations in m6A modification patterns. This underscores the urgent need for comprehensive investigations into these epigenetic factors, as a deeper understanding could lead to enhanced diagnostic markers and innovative therapeutic strategies. The integration of genetic and epigenetic considerations is essential for advancing the field of GC research. This synthesis of recent findings concerning epigenetic regulation offers valuable insights that could inform future studies and therapeutic developments. There is a critical need for ongoing research to elucidate the complexities of epigenetic modifications in GC, ultimately improving patient outcomes through tailored interventions. [ABSTRACT FROM AUTHOR]

Science should provide students an accurate and contemporary education on genetic influence, particularly how it impacts trait variability and developmental norms. Stories involving familial, racial, and sexual differences routinely appear in the popular media and sales of over‐the‐counter genetic tests are mounting. Unfortunately, research suggests genetic curricula in secondary education and university courses have little impact on genetic literacy; instead they appear to amplify genetic essentialism. This position paper reports on genetic essentialism, the impact of three components of science education (teachers, students, curriculum), and critiques existing genetic lessons in two prevalent scientific disciplines, biology and psychology. Two entrenched 19th century genetic paradigms (e.g., Mendelian inheritance and behavioral genetics) are specifically examined. The paper closes with specific recommendations for improving students' genetic literacy including important contemporary genetic science (e.g., epigenetics) and instructional approaches (e.g., learning progression, refutational teaching). [ABSTRACT FROM AUTHOR]

Cancer, a chronic disease characterized by uncontrolled cell development, kills millions of people globally. The WHO reported over 10 million cancer deaths in 2020. Anticancer medications destroy healthy and malignant cells. Cancer treatment induces neuropathy. Anticancer drugs cause harm to spinal cord, brain, and peripheral nerve somatosensory neurons, causing chemotherapy-induced neuropathic pain. The chemotherapy-induced mechanisms underlying neuropathic pain are not fully understood. However, neuroinflammation has been identified as one of the various pathways associated with the onset of chemotherapy-induced neuropathic pain. The neuroinflammatory processes may exhibit varying characteristics based on the specific type of anticancer treatment delivered. Neuroinflammatory characteristics have been observed in the spinal cord, where microglia and astrocytes have a significant impact on the development of chemotherapy-induced peripheral neuropathy. The patient's quality of life might be affected by sensory deprivation, loss of consciousness, paralysis, and severe disability. High cancer rates and ineffective treatments are associated with this disease. Recently, histone deacetylases have become a novel treatment target for chemotherapy-induced neuropathic pain. Chemotherapy-induced neuropathic pain may be treated with histone deacetylase inhibitors. Histone deacetylase inhibitors may be a promising therapeutic treatment for chemotherapy-induced neuropathic pain. Common chemotherapeutic drugs, mechanisms, therapeutic treatments for neuropathic pain, and histone deacetylase and its inhibitors in chemotherapy-induced neuropathic pain are covered in this paper. We propose that histone deacetylase inhibitors may treat several aspects of chemotherapy-induced neuropathic pain, and identifying these inhibitors as potentially unique treatments is crucial to the development of various chemotherapeutic combination treatments. [ABSTRACT FROM AUTHOR]

Plasticity is found in all domains of life and is particularly relevant when populations experience variable environmental conditions. Traditionally, evolutionary models of plasticity are non-mechanistic: they typically view reactions norms as the target of selection, without considering the underlying genetics explicitly. Consequently, there have been difficulties in understanding the emergence of plasticity, and in explaining its limits and costs. In this paper, we offer a novel mechanistic approximation for the emergence and evolution of plasticity. We simulate random "epigenetic mutations" in the genotype–phenotype mapping, of the kind enabled by DNA-methylations/demethylations. The frequency of epigenetic mutations at loci affecting the phenotype is sensitive to organism stress (trait–environment mismatch), but is also genetically determined and evolvable. Thus, the "random motion" of epigenetic markers enables developmental learning-like behaviors that can improve adaptation within the limits imposed by the genotypes. However, with random motion being "goal-less," this mechanism is also vulnerable to developmental noise leading to maladaptation. Our individual-based simulations show that epigenetic mutations can hide alleles that are temporarily unfavorable, thus enabling cryptic genetic variation. These alleles can be advantageous at later times, under regimes of environmental change, in spite of the accumulation of genetic loads. Simulations also demonstrate that plasticity is favored by natural selection in constant environments, but more under periodic environmental change. Plasticity also evolves under directional environmental change as long as the pace of change is not too fast and costs are low. [ABSTRACT FROM AUTHOR]

The Evolutionary Developmental Biology (in abbreviation Evo-Devo) gains in popularity among psychologists. It would be a "synthesis of development and evolution" which would finally allow a rapprochement of psychology and biology. The Evo-Devo redefines epigenetics and opposes it to the (alleged) genetic determinism, genetic reductionism and preformationism of the Modern Synthesis (MS), proposes the concept of the extended inheritance and a mechanism of inheritance of acquired characters, which are claimed to be (neo-) Lamarckian, fuses the three questions separated by the MS: the origin of variation, fate of variation and inheritance of variation. These points of the Evo-Devo's programme particularly resonate with psychologists' expectations: genes alone do not explain the question of transgenerationality, the ontogeny of the attachment, e.g. early experience with caregivers (e.g. separation and loss) have a long-term effects on adult development can span a person's lifetime, can even span generations. However, in the paper I show that the inheritance of acquired characters is indeed impossible, that Lamarck never proposed a theory of the inheritance of acquired characters and that it is a confusion rather than fusion to link the question of the origin of variation, the question of development and the one of inheritance. If the Evo-Devo is so appealing to psychologists, it is not because there is "a new biology for psychology." I show that psychologists' attitude towards monism was ambivalent and such was the relationship between psychology and biology. The paper is a standpoint of a philosopher of biology interested in psychology. [ABSTRACT FROM AUTHOR]

In light of the post-genomic era, epigenetics brings about an opportunity to better understand how the molecular machinery works and is led by a complex dynamic set of mechanisms, often intricate and complementary in many aspects. In particular, epigenetics links developmental biology and genetics, as well as many other areas of knowledge. The present work highlights substantial scopes and relevant discoveries related to the development of the term from its first notions. To our understanding, the concept of epigenetics needs to be revisited, as it is one of the most relevant and multifaceted terms in human knowledge. To redirect future novel experimental or theoretical efforts, it is crucial to compile all significant issues that could impact human and ecological benefit in the most precise and accurate manner. In this paper, the reader can find one of the widest compilations of the landmarks and epistemic considerations of the knowledge of epigenetics across the history of biology from the earliest epigenetic formulation to genetic determinism until the present. In the present work, we link the current body of knowledge and earlier pre-genomic concepts in order to propose a new definition of epigenetics that is faithful to its regulatory nature. [ABSTRACT FROM AUTHOR]

The epigenetic machinery has received extensive attention due to its involvement in plant growth, development, and adaptation to environmental changes. Recent studies often highlight the epigenetic regulatory network by discussing various epigenetic mutants across various plant species. However, a systemic understanding of essential epigenetic regulatory mechanisms remains limited due to a lack of representative mutants involved in multiple biological processes. Colorless Non-ripening (Cnr), a spontaneous epimutant isolated from a commercial population, was initially characterized for its role in fruit ripening regulation. Cnr fruits exhibit an immature phenotype with yellow skin, attributed to hypermethylation of the SQUAMOSA PROMOTER BINDING PROTEIN-LIKECNR (SlSPL-CNR) promoter, resulting in the repression of gene expression. In addition to DNA methylation, this process also involves histone modification and microRNA, integrating multiple epigenetic regulatory factors. Interestingly, knockout mutants of SlSPL-CNR display phenotypical distinctions from Cnr in fruit ripening, indicating complex genetic and epigenetic control over the nonripening phenotype in Cnr fruits. Accumulating evidence suggests that Cnr epimutation is pleiotropic, participating in various biological processes such as Cd stress, Fe deficiency, vivipary, and cell death. Therefore, the Cnr epimutant serve as an excellent model for unveiling how epigenetic mechanisms are involved in diverse biological processes. This review paper focuses on recent research advances regarding the Cnr epimutant, delving into its complex genetic and epigenetic regulatory mechanisms, with the aim of enhancing our understanding and facilitating the development of high-quality, high-yield crops through epigenetic modification. [ABSTRACT FROM AUTHOR]

Simple Summary: Insects, like other animals, must face severe winter low temperature conditions in northern areas. Some insects even freeze entirely and wait out the winter until spring comes. Epigenetic modifications have been suggested to play a vital role in regulating the cold responses of insects. However, the dynamics of the enzymes involved in histone lysine methylation, histone H3 acetylation and methylation in response to cold winters in the freeze-tolerant goldenrod gall fly larvae Eurosta solidaginis and the freeze-avoiding gall moth caterpillars Epiblema scudderiana remains unclear. This paper investigates the modifications of key nuclear proteins that act as gene regulators and mainly focuses on proteins—called histones—that act to depress metabolism. The results indicate that histones are modified in E. solidaginis and Ep. scudderiana during winter. Significant reductions were observed in most of the targets of histone methylation/acetylation for decreasing temperatures of Ep. scudderiana larvae, whereas selected histone methylation/acetylation targets were conversely elevated in E. solidaginis. These epigenetic changes are shown to be an important element in winter survival. Overwintering survival by insects, whether of the freeze-tolerant or freeze-avoiding types, is typically associated with a strong suppression of metabolic rate (e.g., entry into diapause) that involves the differential expression of many genes with regulation at the transcriptional, translational or post-translational levels. Epigenetic modifications have been suggested to play a vital role in regulating cold responses of insects. However, knowledge of the roles of epigenetic mechanisms in modulating gene expression for winter survival of the larvae of two goldenrod gall formers, the freeze-tolerant dipteran Eurosta solidaginis and the freeze-avoiding lepidopteran Epiblema scudderiana, remain unknown. The current study evaluates the role of cold-induced lysine methylation and histone modifications, with enzymes of lysine methylation (SETD8, SETD7, SUV39H1, SMYD2 and ASH2L), as well as relative levels of histone H3 acetylation (H3K9ac, H3K18ac, H3K27ac, H3K56ac) and methylation (H3K4me1, H3K9me3, H3K36me2) examined in two insects. Significant (p < 0.05) reductions were observed in most of the targets of histone methylation/acetylation for decreasing temperatures of Ep. scudderiana larvae, whereas selected histone methylation/acetylation targets were conversely elevated (p < 0.05) in E. solidaginis, particularly under conditions of 5 °C for 4 h. Histone H3 expression was found to be variable without statistical differences in larval goldenrod gall moths and gall flies. These results provide basic information on the patterns of epigenetic regulation involved in insect cold hardiness. [ABSTRACT FROM AUTHOR]

Gliomas are a common type of brain tumor that begins in the glial cells of the brain or spinal cord. IDH1 and IDH2 genes, encoding for the Isocitrate Dehydrogenase (IDH), are frequently mutated in gliomas, which leads to the conversion of aKetoglutarate (a-KG) to 2-Hydroxyglutarate (2-HG). This leads to several epigenetic changes in the genome, further leading to the activation of tumor cells in the brain. The mutation in the IDH1 gene also suppresses the immune system, offering new potential that can lead to the development of drugs and therapies that particularly target and strengthen the immune system. Due to the potential successes of new immunotherapy treatments, gliomas can be treated more effectively. Despite these successes in immunotherapy treatments for gliomas, further research needs to be conducted on the types of mechanisms by which drugs and immunotherapeutic treatments treat different gliomas. Through this paper, I hope to discuss the effects of IDH1 mutation in glioma cells and the potential therapies to treat gliomas. I further wish to discuss the potential benefits of combination therapeutics over monotherapy. [ABSTRACT FROM AUTHOR]

Epigenetics plays a crucial role in various clinical diseases, such as autism, by mediating the impact of environmental variables on genomic regulation. Autism spectrum disorder (ASD) is a neurological disorder influenced by both genetic and environmental factors that affect the developing brain. DNA methylation, histone tail modifications, and noncoding RNA activity can change the function of genes without altering nucleotide sequences. Genes and environment combine to produce the etiology of ASD. One of the main areas of ASD research now being studied is the effects of epigenetic factors on gene expression, such as DNA methylation. Autistic patients exhibit evidence of oxidative stress and impaired methylation, which may reflect the effects of toxic exposure on sulfur metabolism that may lead to cellular damage in the brain and altered expression of epigenetic genes. This review paper summarizes the findings of the supplementary therapy studies of ASD, showing that supplements, including B9, B12, B6, D, E, C, glutathione, omega-3, and choline, are highly effective in modifying methylation in autism, improving many nutrient and metabolic problems, and resulting in significant improvements in symptoms. [ABSTRACT FROM AUTHOR]

Copyright of Frontiers of Information Technology & Electronic Engineering is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

DNA methylation indicates the individual's aging, so-called Epigenetic clocks, which will improve the research and diagnosis of aging diseases by investigating the correlation between methylation loci and human aging. Although this discovery has inspired many researchers to develop traditional computational methods to quantify the correlation and predict the chronological age, the performance bottleneck delayed access to the practical application. Since artificial intelligence technology brought great opportunities in research, we proposed a perceptron model integrating a channel attention mechanism named PerSEClock. The model was trained on 24,516 CpG loci that can utilize the samples from all types of methylation identification platforms and tested on 15 independent datasets against seven methylation-based age prediction methods. PerSEClock demonstrated the ability to assign varying weights to different CpG loci. This feature allows the model to enhance the weight of age-related loci while reducing the weight of irrelevant loci. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Sichuan University (Medical Science Edition) is the property of Editorial Board of Journal of Sichuan University (Medical Sciences) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Epigenetic changes are heritable changes in gene expression without changes in the nucleotide sequence of genes. Epigenetic changes play an important role in the development of cancer and in the process of malignancy metastasis. Previous studies have shown that abnormal epigenetic changes can be used as biomarkers for disease status and disease prediction. The reversibility and controllability of epigenetic modification changes also provide new strategies for early disease prevention and treatment. In addition, corresponding drug development has also reached the clinical stage. In this paper, we will discuss the recent progress and application status of tumor epigenetic biomarkers from three perspectives: DNA methylation, non-coding RNA, and histone modification, in order to provide new opportunities for additional tumor research and applications. [ABSTRACT FROM AUTHOR]

INTRODUCTION: The Developmental Origins of Health and Disease (DOHaD) hypothesis proposes a connection between early life exposures--encompassing the prenatal conditions of sperm, in-utero conditions and thereafter--and long-term metabolic disorders and diseases like diabetes, cancer and neurodevelopmental disorders. This hypothesis suggests that environmental conditions can modulate epigenetic processes, driving DNA changes in response to environment and impacting fetal behaviour.1 For example, epigenetic mechanisms such as histone modifications alter genomic DNA during the embryogenesis stage.2 These alterations in early developmental stages can induce and maintain altered gene expression throughout life, consequently affecting adult pathology.3,4 While a plethora of factors--such as paternal exposures, postnatal environments, and sociocultural factors--also contribute to the DOHaD theory, emphasis is placed on maternal exposures in utero.5 As epigenetics garners media attention, Richardson et al. warn about the impacts of oversimplification and miscommunication of DOHaD, contributing to narratives that unjustly blame mothers for their children's future disease susceptibility.6 This paper will examine the causes, implications, and strategies to address mother-blame narratives pervading DOHaD discourse through a feminist lens, focusing on the experiences of pregnant mothers. [ABSTRACT FROM AUTHOR]

Purpose: To provide a scientific report using peer-reviewed scientific papers that will demonstrate the implications of brain function and plasticity and its correlation to Subluxation and hence the implications of brain function enhancement through chiropractic adjustments. Methods: Analysis was undertaken of the literature reporting on brain plasticity related to brain function and its dependance on chemical changes within the brain. These were found to be highly related to a wide array of clinical outcomes. The literature demonstrates that now we can identify the chemical changes within the brain that are highly related to the same peripheral changes and central nervous system changes that we see with subluxation. Hence, the literature goes on to indicate that correction of these peripheral changes and central nervous system changes will in fact create changes in the biochemical function in the brain affecting brain plasticity for the better. It is inferred that the correction of brain plasticity will have outcomes affecting the entire body including brain function itself improving conditions such as anxiety, depression, addiction, personality conflicts, and learning disabilities. There is a question as well in most literature where it is suggested that changes in the brain chemistry and plasticity could very well aid in other problems such as MS, Alzheimer's, Parkinson's, etc. Conclusions: It is reported here that there is a strong apparent connection between brain plasticity neurochemistry and Subluxation. We put forward that the chiropractic adjustment making changes in this neurochemistry will represent a profound change in brain plasticity, function, and learning. Further studies concerning this topic are needed to further corroborate our observations. [ABSTRACT FROM AUTHOR]

Fetal alcohol spectrum disorders (FASD) represent a continuum of lifelong impairments resulting from prenatal exposure to alcohol, with significant global impact. The "spectrum" of disorders includes a continuum of physical, cognitive, behavioral, and developmental impairments which can have profound and lasting effects on individuals throughout their lives, impacting their health, social interactions, psychological well-being, and every aspect of their lives. This narrative paper explores the intricate relationship between oxidative stress and epigenetics in FASD pathogenesis and its therapeutic implications. Oxidative stress, induced by alcohol metabolism, disrupts cellular components, particularly in the vulnerable fetal brain, leading to aberrant development. Furthermore, oxidative stress is implicated in epigenetic changes, including alterations in DNA methylation, histone modifications, and microRNA expression, which influence gene regulation in FASD patients. Moreover, mitochondrial dysfunction and neuroinflammation contribute to epigenetic changes associated with FASD. Understanding these mechanisms holds promise for targeted therapeutic interventions. This includes antioxidant supplementation and lifestyle modifications to mitigate FASD-related impairments. While preclinical studies show promise, further clinical trials are needed to validate these interventions' efficacy in improving clinical outcomes for individuals affected by FASD. This comprehensive understanding of the role of oxidative stress in epigenetics in FASD underscores the importance of multidisciplinary approaches for diagnosis, management, and prevention strategies. Continued research in this field is crucial for advancing our knowledge and developing effective interventions to address this significant public health concern. [ABSTRACT FROM AUTHOR]

Skeletal muscle is a heterogeneous tissue composed of different types of muscle fibers, demonstrating substantial plasticity. Physiological or pathological stimuli can induce transitions in muscle fiber types. However, the precise regulatory mechanisms behind these transitions remains unclear. This paper reviews the classification and characteristics of muscle fibers, along with the classical mechanisms of muscle fiber type transitions. Additionally, the role of exercise-induced muscle fiber type transitions in disease intervention is reviewed. Epigenetic pathways mediate cellular adaptations and thus represent potential targets for regulating muscle fiber type transitions. This paper focuses on the mechanisms by which epigenetic modifications couple mitochondrial function and contraction characteristics. Reactive Oxygen Species (ROS) are critical signaling regulators for the health-promoting effects of exercise. Finally, we discuss the role of exercise-induced ROS in regulating epigenetic modifications and the transition of muscle fiber types. [Display omitted] • Contractile property couples to metabolic capacity in muscle fiber type transition. • Epigenetic machinery couples muscle contractile property to mitochondrial function. • Exercise modulates epigenetic machinery through the ROS/AMPK pathway. [ABSTRACT FROM AUTHOR]

Simple Summary: This review mainly focuses on epigenetic changes in a few selective genes associated with insulin insensitivity in the periphery and how this peripheral insulin insensitivity is linked with impaired signaling of insulin in the brain, thus causing Alzheimer's disease. DNA methylation and histone modifications are the focus of this review, with primary importance given to DNA methylation. Moreover, there has been a focus shift from the amyloid β hypothesis to epigenetic mechanisms. Furthermore, we discuss the advanced drug delivery systems that can be used for the delivery of drugs targeting the brain during Alzheimer's disease. The advanced drug delivery systems discussed in this paper are nanoparticles, vesicular systems, network systems and dendrimers, hydrogel-based systems, and biologics. Alzheimer's disease (AD) is a neurodegenerative condition that predominantly affects the hippocampus and the entorhinal complex, leading to memory lapse and cognitive impairment. This can have a negative impact on an individual's behavior, speech, and ability to navigate their surroundings. AD is one of the principal causes of dementia. One of the most accepted theories in AD, the amyloid β (Aβ) hypothesis, assumes that the buildup of the peptide Aβ is the root cause of AD. Impaired insulin signaling in the periphery and central nervous system has been considered to have an effect on the pathophysiology of AD. Further, researchers have shifted their focus to epigenetic mechanisms that are responsible for dysregulating major biochemical pathways and intracellular signaling processes responsible for directly or indirectly causing AD. The prime epigenetic mechanisms encompass DNA methylation, histone modifications, and non-coding RNA, and are majorly responsible for impairing insulin signaling both centrally and peripherally, thus leading to AD. In this review, we provide insights into the major epigenetic mechanisms involved in causing AD, such as DNA methylation and histone deacetylation. We decipher how the mechanisms alter peripheral insulin signaling and brain insulin signaling, leading to AD pathophysiology. In addition, this review also discusses the need for newer drug delivery systems for the targeted delivery of epigenetic drugs and explores targeted drug delivery systems such as nanoparticles, vesicular systems, networks, and other nano formulations in AD. Further, this review also sheds light on the future approaches used for epigenetic drug delivery. [ABSTRACT FROM AUTHOR]

Omics technologies accumulated an enormous amount of data that advanced knowledge about the molecular pathogenesis of type 1 diabetes mellitus and identified a number of fundamental problems focused on the transition to personalized diabetology in the future. Among them, the most significant are the following: (1) clinical and genetic heterogeneity of type 1 diabetes mellitus; (2) the prognostic significance of DNA markers beyond the HLA genes; (3) assessment of the contribution of a large number of DNA markers to the polygenic risk of disease progress; (4) the existence of ethnic population differences in the distribution of frequencies of risk alleles and genotypes; (5) the infancy of epigenetic research into type 1 diabetes mellitus. Disclosure of these issues is one of the priorities of fundamental diabetology and practical healthcare. The purpose of this review is the systemization of the results of modern molecular genetic, transcriptomic, and epigenetic investigations of type 1 diabetes mellitus in general, as well as its individual forms. The paper summarizes data on the role of risk HLA haplotypes and a number of other candidate genes and loci, identified through genome-wide association studies, in the development of this disease and in alterations in T cell signaling. In addition, this review assesses the contribution of differential DNA methylation and the role of microRNAs in the formation of the molecular pathogenesis of type 1 diabetes mellitus, as well as discusses the most currently central trends in the context of early diagnosis of type 1 diabetes mellitus. [ABSTRACT FROM AUTHOR]

This document is an editorial for a special issue of the International Journal of Molecular Sciences focused on neurodevelopmental disorders. The editorial highlights the complex mechanisms underlying these disorders, which impact both childhood and adult life. It discusses the six primary diseases within this classification group, including Intellectual Disability, Communication Disorders, Autism Spectrum Disorder, Attention-Deficit/Hyperactivity Disorder, Neurodevelopmental Motor Disorders, and Specific Learning Disorders. The editorial emphasizes the importance of understanding the genetic causes and epigenetic changes associated with these disorders for future prevention strategies. The special issue includes original research papers, a communication, and informative review articles that provide comprehensive insights into neurodevelopmental disorders. [Extracted from the article]

Some genes carry an ‘imprint’ on either the maternal or the paternal copy, which determines whether or not that copy is expressed. This 1984 discovery changed how scientists think about gene regulation and inheritance.Landmark 1984 experiments gave rise to a new epigenetics concept. [ABSTRACT FROM AUTHOR]

Background: Currently, the prevalence of Alzheimer's disease (AD) is progressively rising, particularly in developed nations. There is an escalating focus on the onset and progression of AD. A mounting body of research indicates that epigenetics significantly contributes to AD and holds substantial promise as a novel therapeutic target for its treatment. Objective: The objective of this article is to present the AD areas of research interest, comprehend the contextual framework of the subject research, and investigate the prospective direction for future research development. Methods: ln Web of Science Core Collection (WOSCC), we searched documents by specific subject terms and their corresponding free words. VOSviewer, CiteSpace and Scimago Graphica were used to perform statistical analysis on measurement metrics such as the number of published papers, national cooperative networks, publishing countries, institutions, authors, co-cited journals, keywords, and visualize networks of related content elements. Results: We selected 1,530 articles from WOSCC from January 2013 to June 2023 about epigenetics of AD. Based on visual analysis, we could get that China and United States were the countries with the most research in this field. Bennett DA was the most contributed and prestigious scientist. The top 3 cited journals were Journal of Alzheimer's Disease, Neurobiology of Aging and Molecular Neurobiology. According to the analysis of keywords and the frequency of citations, ncRNAs, transcription factor, genome, histone modification, blood DNA methylation, acetylation, biomarkers were hot research directions in AD today. Conclusion: According to bibliometric analysis, epigenetic research in AD was a promising research direction, and epigenetics had the potential to be used as AD biomarkers and therapeutic targets. [ABSTRACT FROM AUTHOR]

Periodontitis (PD) is a prevalent and chronic inflammatory disease with a complex pathogenesis, and it is associated with the presence of specific pathogens, such as Porphyromonas gingivalis. Dysbiosis and dysregulated immune responses ultimately lead to chronic inflammation as well as tooth and alveolar bone loss. Multiple studies have demonstrated that genetic polymorphisms may increase the susceptibility to PD. Furthermore, gene expression is modulated by various epigenetic mechanisms, such as DNA methylation, histone modifications, or the activity of non-coding RNA. These processes can also be induced by PD-associated pathogens. In this review, we try to summarize the genetic processes that are implicated in the pathogenesis of PD. Furthermore, we discuss the use of these mechanisms in diagnosis and therapeutic purposes. Importantly, novel treatment methods that could promote tissue regeneration are greatly needed in PD. In this paper, we also demonstrate current evidence on the potential use of stem cells and extracellular vesicles to stimulate tissue regeneration and suppress inflammation. The understanding of the molecular mechanisms involved in the pathogenesis of PD, as well as the impact of PD-associated bacteria and stem cells in these processes, may enhance future research and ultimately improve long-term treatment outcomes. [ABSTRACT FROM AUTHOR]

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease in which immune disorders lead to autoreactive immune responses and cause inflammation and tissue damage. Genetic and environmental factors have been shown to trigger SLE. Recent evidence has also demonstrated that epigenetic factors contribute to the pathogenesis of SLE. Epigenetic mechanisms play an important role in modulating the chromatin structure and regulating gene transcription. Dysregulated epigenetic changes can alter gene expression and impair cellular functions in immune cells, resulting in autoreactive immune responses. Therefore, elucidating the dysregulated epigenetic mechanisms in the immune system is crucial for understanding the pathogenesis of SLE. In this paper, we review the important roles of epigenetic disorders in the pathogenesis of SLE. [ABSTRACT FROM AUTHOR]

The present study is based on the analysis and conclusions in a preceding paper by the author. Major interpretations of epigenetics are considered - social-ecological, biomedical and bioethical, - as well as their impact on social sciences and humanities, policies and opportunities for human development. The following important conclusions are formulated: firstly, epigenetics can be a stimulus to reform social sciences, as well as for policies aiming at purer environment, less poverty and social inequality, more freedom and less violence; (2) one-sided and implicit biomedical interpretation of epigenetics not only does not solve but intensifies existing problems relating to health and wellbeing of people in contemporary societies; (3) this however does not mean rejecting the biomedical approach but finding it's appropriate and balanced place in the context of functioning ecological and social policies; (4) practices and behavioural models that epigenetics determines as sensitive presuppose respective responsibilities on the part of various subjects - organisations, institutions and pdrticular individuals. A critical evaluation is necessary of attempts to reject responsibilities as well as of their imballanced distribution among various subjects. [ABSTRACT FROM AUTHOR]

Emerging evidence that intrauterine exposures to environmental stressors can ‘programme’ epigenetic modifications in offspring, leading to long‐lasting health risks, has generated debate about whether prospective mothers have a specific ‘epigenetic’ moral responsibility. However, to date, proposals for maternal epigenetic responsibility have failed to grapple adequately with the uncertainty of scientific evidence, and specifically, whether the causal basis for intrauterine epigenetic effects is sufficiently established to ground claims of moral responsibility. Causality is widely considered a necessary condition for the attribution of moral responsibility. In this paper, we show that much foetal programming science in humans has yet to establish a causal epigenetic connection between intrauterine exposures and subsequent offspring health impacts. This research struggles to establish that the relationship between such exposures and offspring health risks is in fact causal, neither has it been able to evince the causal significance of exposures during pregnancy to such outcomes. We argue that these two challenges to establishing causality in foetal programming research seriously undercut the idea that prospective mothers may have a moral responsibility to ensure the epigenetics of their offspring. [ABSTRACT FROM AUTHOR]

Psoriasis is an immune‐mediated, inflammatory disease. Genetic and environmental elements are involved in the nosogenesis of this illness. Epigenetic inheritance serves as the connection between genetic and environmental factors. Histone modification, an epigenetic regulatory mechanism, is implicated in the development of numerous diseases. The basic function of histone modification is to regulate cellular functions by modifying gene expression. Modulation of histone modification, such as regulation of enzymes pertinent to histone modification, can be an alternative approach for treating some diseases, including psoriasis. Herein, we reviewed the regulatory mechanisms and biological effects of histone modifications and their roles in the pathogenesis of psoriasis. This paper reviewed the regulatory mechanisms and biological effects of histone modifications and their roles in the pathogenesis of psoriasis. It highlights the role of epigenetic inheritance and the potential of targeting histone modification as an alternative therapeutic approach for psoriasis and other‐related diseases. [ABSTRACT FROM AUTHOR]

Epigenetics in the form of DNA methylation and other processes is an established property of genotypes and a focus of empirical research. Yet, there remain fundamental gaps in the evolutionary theory of epigenetics. To support a comprehensive understanding of epigenetics, this paper investigates theoretically the combined effects of deleterious mutation and epimutation with and without inbreeding. Both spontaneous epimutation and paramutation are considered to cover a broader range of epigenetic phenomena. We find that inbreeding generally reduces the amount of segregating deleterious genetic and epigenetic variation at equilibrium, although interestingly inbreeding can also increase the amount of deleterious genetic or epigenetic variation. Furthermore, we also demonstrate that epimutation indirectly can cause increased or decreased deleterious genetic variation at equilibrium relative to classic expectations, which is particularly evident when paramutation is occurring. With the addition of deleterious epimutation, there may be significantly increased purging of deleterious variation in more inbred populations and a significantly increased amount of segregating deleterious variation in more outbred populations, with notable exceptions. [ABSTRACT FROM AUTHOR]

Background: Gut microbiota is an important factor affecting host health. With the further study of the mechanism of gut microbiota, significant progress has been made in the study of the link between gut microbiota and epigenetics. This study visualizes the body of knowledge and research priorities between the gut microbiota and epigenetics through bibliometrics. Methods: Publications related to gut microbiota and epigenetics were searched in the Web of Science Core Collection (WoSCC) database. Vosviewer 1.6.17 and CiteSpace 6.1.R2 were used for bibliometric analysis. Results: WoSCC includes 460 articles from 71 countries. The number of publications on gut microbiota and epigenetics has increased each year since 2011. The USA, PEOPLES R CHINA, and ITALY are at the center of this field of research. The University of California System, Harvard University, and the University of London are the main research institutions. Li, X, Yu, Q, Zhang, S X are the top authors in this research field. We found that current research hotspots and frontiers include short-chain fatty acids (SCFA) play an important role in gut microbiota and epigenetic mechanisms, gut microbiota and epigenetics play an important role in host obesity, diet, and metabolism. Gut microbiota and epigenetics are closely related to colorectal cancer, breast cancer, and inflammatory bowel disease. At the same time, we found that gut microbiota regulates epigenetics through the gut-brain axis and has an impact on psychiatric diseases. Therefore, probiotics can regulate gut microbiota, improve lifestyle, and reduce the occurrence and development of diseases. Conclusion: This is the first comprehensive and in-depth bibliometric study of trends and developments in the field of gut microbiota and epigenetics research. This study helps to guide the direction of research scholars in their current field of study. [ABSTRACT FROM AUTHOR]

Introduction: Klotho is a membrane protein predominantly expressed in the kidneys, and its discovery was serendipitously made through gene-targeting experiments conducted on mice. Klotho has a favorable role in the regulation of multiple cellular processes, such as aging, oxidative stress, inflammation, and apoptosis. This regulation occurs through the targeting of diverse signaling molecules, cell membrane receptors, and ion channels, achieved by physical contacts or enzymatic activities of Klotho. This review examines the role of Klotho in the epigenetic regulation of molecules associated with diabetes. Methods: Authors conducted a thorough literature search using the PubMed®, Web of Science™, and Scopus®. Relevant articles up to September 2023, published in the English language were considered. We reviewed research databases searching for studies that included keywords klotho, epigenetic, and diabetes. Results: 14 related papers about epigenetic modification of proteins involved in diabetes pathogenesis were selected to be included in this narrative review. In the studies, the kidney was the most investigated organ regarding this correlation. Also, phosphorylation and methylation were the common epigenetic modifications of proteins by Klotho. Conclusion: Klotho has a significant role in the maturation of adipocytes and the regulation of systemic glucose metabolism, exhibiting a strong association with the pathogenesis of diabetes. Both epigenetic alterations and the modulation of protein phosphorylation by Klotho play significant roles in the regulation of Klotho expression and the modulation of other molecules implicated in the etiology of diabetes. [ABSTRACT FROM AUTHOR]

MAGUK p55 subfamily member 7, a part of the membrane palmitoylated protein subfamily, is an essential adapter that promotes epithelial cell polarity and has increasing significance in multiple cancers, including esophageal cancer, clear cell renal cell carcinoma, breast cancer, and pancreatic ductal adenocarcinoma. This paper aims to determine the effect of the MAGUK p55 subfamily member 7 in various tumor types using The Cancer Genome Atlas and Genotype-Tissue Expression database. A variety of software and web platforms, such as cBioPortal, GEPIA2, TIMER2, UALCAN, R, STRING, and DAVID, were used to obtain and analyze data. Notably, low expression of MAGUK p55 subfamily member 7 was observed in most cancers. In addition, low expression of MAGUK p55 subfamily member 7 predicted poor prognoses in cancer patients. Mutation was the most frequent genetic alteration type in MAGUK p55 subfamily member 7, with the phosphorylation sites identified as S412 and S490 in various cancers. Furthermore, expression of MAGUK p55 subfamily member 7 was associated with cancer-related fibroblasts and CD8+ T cells. Gene enrichment analysis indicated that MAGUK p55 subfamily member 7 influences cancer through the Rap1 signaling pathway. This paper elucidates the biological significance of MAGUK p55 subfamily member 7 in human pan-cancer prognosis and immune response.

Background: Lung cancer is a highly prevalent cancer on a global scale and its oncogenic process is driven by the accumulation of multiple pathological events. Epigenetics has gained significant recognition in recent years as a crucial contributor to the development of lung cancer. Epigenetics include processes such as DNA methylation, histone modification, chromatin remodeling, and RNA modification. These pathways lead to enduring alterations in genetic phenotypes, which are crucial in the advancement and growth of lung cancer. However, the specific mechanisms and roles of epigenetics in lung cancer still need to be further elucidated. Methods: We obtained publications from the Web of Science databases and applied a rigorous search method to filter them. Ultimately, we gathered high-quality publications that had received the highest 100 number of citations. The data were processed and visualized by various bibliometric tools. Results: The 100 papers had varying numbers of citations, with the lowest being 491 and the most being 6316. On average, each work received 1119 citations. A total of 1056 co-authors were involved in publishing these papers in 59 journals from 185 institutions in 27 countries. The majority of high-caliber research in the subject of lung cancer epigenetics is conducted in advanced countries, with the United States taking the lead in terms of both the quantity of articles produced and their academic influence. The study of DNA methylation has been a longstanding research priority in the discipline. With the development of next-generation sequencing technology in recent years, research related to non-coding RNA has become a research hotspot. Future research directions may focus more on exploring the mechanisms of action of messenger RNA and circular RNA and developing targeted treatment strategies based on non-coding RNA drugs. Conclusion: We analyzed 100 top lung cancer and epigenetics documents through various bibliometric analysis tools. This study provides a concise overview of the findings from prior research, anticipates future research directions, and offers potential avenues for additional investigation.

The Molecular Transducers of Physical Activity Consortium (MoTrPAC) aims to comprehensively map molecular alterations in response to acute exercise and chronic training. In one of a recent series of papers from MoTrPAC, Nair et al. provide the first multi-epigenomic and transcriptomic integration across eight tissues in both sexes following adaptation to endurance exercise training (EET). [ABSTRACT FROM AUTHOR]

Aims. To investigate DNA methylation of specific gene promoters in endometrial hyperplasia compared to normal endometrial tissue. Materials and Methods. To search for epigenetic events, methylation-specific multiplex ligation-dependent probe amplification was employed to compare the methylation status of 64 tissue samples with atypical endometrial hyperplasia, 60 tissue samples with endometrial hyperplasia without atypia, and 40 control tissue samples with normal endometrium. Results. Differences in DNA methylation among the groups were found in PTEN, CDH13, and MSH6 promoters (PTEN: atypical hyperplasia 32%, benign hyperplasia 6.8%, normal endometrium 10%; P=0.004; CDH13: atypical hyperplasia, 50%; benign hyperplasia, 43%; normal endometrium 8.1%; P=0.003; MSH6 atypical hyperplasia 84%, benign hyperplasia, 62%; normal endometrium, 52%; P=0.008.) Higher rates of CDH13 promoter methylation were identified in the groups with both forms of endometrial hyperplasia when compared to the control group (atypical hyperplasia, P=0.003, benign hyperplasia, P=0.0002). A higher rate of DNA methylation of the PTEN and MSH6 promoters was observed in samples with atypical endometrial hyperplasia than in samples with benign endometrial hyperplasia (PTEN: P=0.02; MSH6: P=0.01) and samples with normal endometrial tissue (PTEN, P=0.04; MSH6, P=0.006). Conclusion. DNA methylation of CDH13, PTEN, and MSH6 appear to be involved in the development of endometrial hyperplasia.