Search Results (80)

Human life expectancy has risen dramatically in the last century, but this demographic triumph has come at the cost of an explosion of non-communicable diseases (NCDs), threatening the sustainability of healthcare systems in aging, low-fertility societies. Evolutionary medicine provides a framework to understand, at least in part, this paradox. Many vulnerabilities to disease are not failures of design but the predictable outcomes of evolutionary trade-offs, constraints, and mismatches. Evolutionary mismatch theory explains how traits once advantageous in ancestral environments become maladaptive in modern contexts of abundance, sedentarism, and urbanization. The developmental origins of health and disease (DOHaD) concept describes how epigenetic plasticity in early life can buffer or amplify these mismatches, depending on whether adult environments align with developmental forecasts. Transgenerational epigenetic inheritance, even if still debated in humans, may further influence phenotypic plasticity, increasing or mitigating the mismatch. In evolutionary terms, the theories of mutation accumulation, antagonistic pleiotropy, and the disposable soma explain why longer lifespans, and ecological and social conditions profoundly different from those in which we developed, increase the likelihood that these costs are expressed clinically. Because most NCDs can be prevented and effectively controlled but not cured, efforts should prioritize quality of life for people, families, and communities. At the individual level, aligning lifestyles with evolved biology can mitigate risk, but the greatest leverage lies in population-level interventions. Urban health strategies represent a forward-looking attempt to realign modern environments with human biology. In this way, the concept of the evolutionary misfit becomes not just a diagnosis of maladaptation, but a guide for building healthier, more sustainable societies. Full article

The global aquaculture industry produces 91 million tons annually, yet achieving sustainable growth optimization remains constrained by incomplete understanding of regulatory system integration, polyploid genomic complexity, and disconnected molecular-environmental approaches. This systematic review synthesizes 180 peer-reviewed articles (1992–2025) from four databases, revealing that growth regulation operates through integrated multi-level networks: the GH-IGF axis, TGF-β/myostatin signaling, and epigenetic mechanisms responding dynamically to environmental inputs. Research acceleration is evident, with 52.2% of studies published during 2020–2025. Whole-genome duplication events created expanded gene repertoires enabling sophisticated regulatory control while presenting breeding challenges in polyploid species. CRISPR-Cas9 myostatin knockout achieves 15–30% growth enhancement, though practical implementation faces regulatory and economic barriers. DNA methylation and microRNAs enable environmental adaptation and transgenerational trait inheritance, offering complementary approaches to conventional breeding. Climate-resilient strain development requires integrating polyploid breeding methodologies, multi-omics phenotyping platforms, and validated epigenetic markers. Sustainable aquaculture intensification through precision genetics demands coordinated infrastructure development, harmonized regulatory frameworks, and international collaboration to address food security while adapting to climate change. This synthesis establishes research priorities bridging molecular mechanisms with practical applications for sustainable production enhancement. Full article

Studies have widely indicated that the composition of maternal nutrition and diets might affect offspring health later in life. Studies on paternal contribution to the offspring’s disease are relatively scarce but are an important subject to the field. Recent research has suggested that paternal factors influenced by nutrition have been implicated in the transgenerational heritage of health and diseases through epigenetic mechanisms. This review aims to explore the current state of knowledge on nutrition-based paternal impacts on gynecological disease through epigenetics, focusing on the transmission of cancer and metabolic diseases from father to female offspring. We will explore the various mechanisms by which epigenetic landmarks, such as DNA methylation, histone modifications, and non-coding RNAs, are passed on through sperm and reprogrammed in the embryo, influencing offspring development and health. We will discuss the impacts of preconception paternal nutrition on two common cancer such as breast cancer and ovarian cancer in female offspring. Additionally, paternal overweight or obesity has been associated with increased risk of obesity in the offspring and compromised metabolic health, which may link to reproductive conditions such as infertility. Understanding the molecular mechanisms underlying non-genetic inheritance is crucial for elucidating the nutrition-mediated developmental origins of health and disease. This review highlights the mechanistic correlation between preconception paternal nutrition and female offspring gynecological health. Furthermore, it emphasizes the need for additional research to establish evidence-based paternal nutrition consultation and guidelines aimed at optimizing reproductive health and pregnancy outcomes in couples planning to conceive. Full article

Introduction: Cigarette smoking is unquestionably associated with an increase in morbidity and mortality worldwide, exerting significant adverse effects on respiratory health. The impact of tobacco persists in the epigenome long after smoking cessation. Furthermore, the offspring of smokers may also be affected by the detrimental effects of smoking. Material and methods: The modifications made to the body, such as DNA methylation, histone modification, and regulation by non-coding RNAs, do not change the DNA sequence but can influence gene expression. In respiratory disease, multigenerational effects have been reported in humans, with an increased risk of asthma or COPD and decreased lung function in offspring, despite them not being exposed to smoke. Prenatal nicotine exposure leads to pulmonary pathology that persists across three consecutive generations, supported by animal studies conducted by Rehan et al. Significant advances in high-throughput genomic and epigenomic technologies have enabled the discovery of molecular phenotypes. These either reflect or are influenced by them. Due to the hidden environmental effects and the rise of artificial intelligence (AI) in biomedical research, new predictive models are emerging that not only explain complex data but also enable earlier detection and prevention of smoking-related diseases. In this narrative review, we synthesise the latest research on how smoking affects gene regulation and chromatin structure, emphasising how tobacco can increase vulnerability to multiple diseases. Discussion: For many years, it was widely believed that diseases are solely inherited through genetics. However, recent research in epigenetics has led to a significant realisation: environmental factors play a crucial role in an individual’s life. External influences leave a mark on DNA that can influence future health and offer insights into potential illnesses. In this context, it is possible that in the future, doctors might treat people not as a whole but as individual beings, with personalised medication, tests, and other approaches. Conclusions: The accumulated evidence suggests that exposure to various environmental factors is associated with multigenerational changes in gene expression patterns, which may contribute to increased disease risk. The application of artificial intelligence in this domain is currently a crucial tool for researching potential future health issues in individuals, and it holds a powerful prospect that could transform current medical and scientific practice. Full article

Plants have evolved a complex, multilayered immune system that integrates molecular recognition, signaling pathways, epigenetic regulation, and small RNA-mediated control. Recent studies have shown that DNA-level regulatory mechanisms, such as RNA-directed DNA methylation (RdDM), histone modifications, and chromatin remodeling, are critical for modulating immune gene expression, allowing for rapid and accurate pathogen-defense responses. The epigenetic landscape not only maintains immunological homeostasis but also promotes stress-responsive transcription via stable chromatin modifications. These changes contribute to immunological priming, a process in which earlier exposure to pathogens or abiotic stress causes a heightened state of preparedness for future encounters. Small RNAs, including siRNAs, miRNAs, and phasiRNAs, are essential for gene silencing before and after transcription, fine-tuning immune responses, and inhibiting negative regulators. These RNA molecules interact closely with chromatin features, influencing histone acetylation/methylation (e.g., H3K4me3, H3K27me3) and guiding DNA methylation patterns. Epigenetically encoded immune memory can be stable across multiple generations, resulting in the transgenerational inheritance of stress resilience. Such memory effects have been observed in rice, tomato, maize, and Arabidopsis. This review summarizes new findings on short RNA biology, chromatin-level immunological control, and epigenetic memory in plant defense. Emerging technologies, such as ATAC-seq (Assay for Transposase-Accessible Chromatin using Sequencing), ChIP-seq (Chromatin Immunoprecipitation followed by Sequencing), bisulfite sequencing, and CRISPR/dCas9-based epigenome editing, are helping researchers comprehend these pathways. These developments hold an opportunity for establishing epigenetic breeding strategies that target the production of non-GMO, stress-resistant crops for sustainable agriculture. Full article

Transgenerational epigenetic inheritance has emerged as a compelling mechanism by which early-life stress can shape behavior in descendants with no direct exposure to trauma. However, whether such heritable modifications affect subtle behavioral phenotypes, like processing of social and emotional stimuli, remains poorly understood. In this study, we investigated the behavioral profile of fourth-generation heterozygous dopamine-transporter (DAT-HET) rats. Compared to control (SX) rats, our experimental group (labelled SIKK) consisted of animals (at G4, F3) born from MIK sires (at G3, F2), who descended from grand-dams (at G2, F1) who were in turn exposed to early-life maltreatment by their own DAT-KO mothers (the great-grand-dams, at G1, F0). To probe inhibitory control and social cognition, we employed the signaled licking / avoidance of punishment (SLAP) task, the elicited preference test (EPT), and the social recognition test (SRT). In the SLAP task, SIKK rats exhibited slower acquisition of passive avoidance, suggesting dampened sensitivity to predictive aversive cues. In the EPT, wild-type focal rats displayed a clear preference for SX over SIKK conspecifics, indicating reduced social appeal of epigenetically altered animals. In the SRT, SX rats successfully discriminated between a novel and a familiar DAT-KO conspecific, while SIKK rats failed to do so, revealing impaired social cognition. Together, these findings indicate that, despite the absence of direct trauma in their infancy, SIKK rats exhibit a distinct behavioral phenotype characterized by increased reactivity to threat and deficits in social preferences and cognition. These alterations reflect inherited dysfunctions in limbic dopaminergic circuits, particularly within PFC. Our study highlights how an ancestor’s adversity can shape adaptive behavior in future generations, providing a powerful model for understanding the biological basis of vulnerability to psychiatric disorders. Full article

Environmental pollutants such as heavy metals, endocrine-disrupting chemicals, microplastics, and airborne particulates are increasingly recognized for their potential to influence immune function through epigenetic mechanisms. This review examines conserved pollutant-associated pathways at interfaces of immunity and epigenetics, with particular attention to Toll-like receptor–NF-κB signalling, NLRP3 inflammasome activity, and reactive oxygen species-driven cascades. Evidence from cellular, animal, and epidemiological studies indicates that these pathways may converge on chromatin regulators such as DNA methyltransferases, histone deacetylases, and EZH2, leading to DNA methylation shifts, histone modifications, and altered chromatin accessibility. Pollutants are also reported to modulate non-coding RNAs, including miR-21, miR-155, and several lncRNAs, which can act as intermediaries between cytokine signalling and epigenetic remodelling. Findings from transgenerational models suggest that pollutant-linked immune–epigenetic alterations might persist across generations, raising the possibility of long-term consequences for immune and neurodevelopmental health. Comparative analyses further indicate convergence across diverse pollutant classes, pointing to a shared mechanistic axis of immune–epigenetic disruption. Overall, these insights suggest that pollutant-induced immune–epigenetic signatures may contribute to inflammation, altered immune responses, and heritable disease risks, and their clarification could inform biomarker discovery and future precision approaches in immunotoxicology. Full article

Drug abuse is a chronic, relapsing disorder marked by compulsive drug-seeking behavior and profound neurobiological consequences. Each year, millions of individuals face serious social and legal repercussions due to addiction. This review synthesizes findings from both preclinical and clinical studies to examine how chronic exposure to substances such as alcohol, cocaine, methamphetamine, and opioids affects the central nervous system. Specifically, it explores the epigenetic modifications induced by these substances, including DNA methylation, histone modifications, and noncoding RNA regulation. The literature was selected using a thematic approach, emphasizing substance-specific mechanisms and their effects on gene expression, synaptic plasticity, and the brain’s reward circuitry. Emerging evidence links these epigenetic changes to long-term behavioral adaptations and even transgenerational inheritance. This review underscores the complex molecular pathways contributing to addiction, vulnerability, and relapse, offering insights into potential therapeutic targets. Full article

Quaternary ammonium compounds (QACs) are a class of chemicals used for their antimicrobial, surfactant, and antistatic properties. QACs are present in many consumer products, and people are regularly exposed to them. We have previously shown reproductive toxicity in mice exposed to the disinfectants alkyl dimethyl benzyl ammonium chloride (ADBAC) and dodecyl dimethyl ammonium chloride (DDAC). To assess the long-term reproductive impacts, a generational reproductive study was conducted. Sperm parameters were determined by CASA and epigenetic enzyme mRNA expression was determined by pathway-focused RT-PCR. Mice ambiently exposed to ADBAC+DDAC exhibited decreases in reproductive indices that persisted through the F1 generation. Male mice (F0) dosed with 120 mg/kg/day of ADBAC+DDAC exhibited decreased sperm concentration and motility that persisted through the F1 generation. Changes in the mRNA expression of chromatin-modifying enzymes in the testes were seen. Two histone acetyltransferases (Hat1 and Kat2b) were upregulated, and one lysine-specific demethylase (Kdm6b) was downregulated in the F0 generation. The DNA methyltransferase Dnmt1 was downregulated in F1 males. These changes in chromatin-modifying enzymes are known to decrease fertility and could be a mechanism for ADBAC+DDAC reproductive toxicity. In all experiments, the F2 generation was similar to the controls, showing multi-generational but not trans-generational epigenetic inheritance. Full article

The epigenetic landscape plays a pivotal role in regulating the functions of both germ and somatic cells (Sertoli and Leydig cells) within the testis, which are essential for male fertility. While somatic cells support germ cell maturation and testosterone synthesis, the epigenetic regulation of germ cells is critical for proper spermatogenesis and function. Epigenetic modifications such as DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs (ncRNAs) are crucial for regulating gene expression that is essential for spermatogenesis and reproductive function. Although numerous studies have highlighted the significance of the epigenome and its implications for male reproductive health, a comprehensive overview of the existing literature and knowledge is lacking. This review aims to provide an in-depth analysis of the role of epigenetics in spermatogenesis and reproductive health, with a specific focus on DNA methylation, histone remodeling, and small noncoding RNAs (sncRNAs). Additionally, we examine the impact of lifestyle and environmental factors, such as diet, smoking, physical activity, and exposure to endocrine-disrupting chemicals, on the sperm epigenome. We emphasize how these factors influence fertility, embryonic development, and potential transgenerational inheritance. This review underscores how recent advances in the understanding of the epigenetic modulation of testicular function can inform the pathophysiology of male infertility, thereby paving the way for the development of targeted diagnostic and therapeutic strategies. Full article

Methylation is a biochemical process involving the addition of methyl groups to proteins, lipids, and nucleic acids (both DNA and RNA). DNA methylation predominantly occurs on cytosine and adenine nucleobases, and the resulting products—most frequently 5-methylcytosine and N⁶-methyladenine epigenetic marks—can significantly influence gene activity at the affected genomic sites without modifying the DNA sequence called nucleotide order. Various environmental factors can alter the DNA methylation pattern. Among these, methyl donor micronutrients, such as specific amino acids, choline, and several B vitamins (including folate, pyridoxine, thiamine, riboflavin, niacin, and cobalamin), primarily regulate one-carbon metabolism. This molecular pathway stimulates glutathione synthesis and recycles intracellular methionine. Glutathione plays a pivotal role during oocyte activation by protecting against oxidative stress, whereas methionine is crucial for the production of S-adenosyl-L-methionine, which serves as the universal direct methyl donor for cellular methylation reactions. Because local DNA methylation patterns at genes regulating fertility can be inherited by progeny for multiple generations even in the absence of the original disrupting factors to which the parent was exposed, and DNA methylation levels at specific genomic sites highly correlate with age and can also be passed to offspring, nutrition can influence reproduction and life span in a transgenerational manner. Full article

Environmental xenobiotics, including heavy metals, endocrine-disrupting chemicals (EDCs), pesticides, air pollutants, nano- and microplastics, mycotoxins, and phycotoxins, are widespread compounds that pose significant risks to human health. These substances, originating from industrial and agricultural activities, vehicle emissions, and household products, disrupt cellular homeostasis and contribute to a range of diseases, including cancer and neurodegenerative diseases, among others. Emerging evidence indicates that epigenetic alterations, such as abnormal deoxyribonucleic acid (DNA) methylation, aberrant histone modifications, and altered expression of non-coding ribonucleic acids (ncRNAs), may play a central role in mediating the toxic effects of environmental xenobiotics. Furthermore, exposure to these compounds during critical periods, such as embryogenesis and early postnatal stages, can induce long-lasting epigenetic alterations that increase susceptibility to diseases later in life. Moreover, modifications to the gamete epigenome can potentially lead to effects that persist across generations (transgenerational effects). Although these modifications represent significant health risks, many epigenetic alterations may be reversible through the removal of the xenobiotic trigger, offering potential for therapeutic intervention. This review explores the relationship between environmental xenobiotics and alterations in epigenetic signatures, focusing on how these changes impact human health, including their potential for transgenerational inheritance and their potential reversibility. Full article

Despite two extensive reprogramming events during early embryogenesis and gametogenesis, epigenetic information can be passed to the next generations, which constitutes the transgenerational epigenetic inheritance of phenotypes. Considering its utmost importance, there have been few studies focused on the transgenerational effects of dietary interventions, such as methionine supplementation, in livestock. Using whole-genome bisulfite sequencing, we implemented a single-base resolution differential methylation analysis for the F3 and F4 descendants of control vs. methionine-supplemented F0 twin-pair rams. Based on the results of our previous study on F0, F1, and F2 generations, we compared current results of 2981 and 1726 differentially methylated cytosines (DMCs), as well as 798 and 553 unique differentially methylated genes (DMGs), in F3 and F4, respectively. We identified 41 DMGs that exhibited transgenerational epigenetic inheritance (TEI-DMGs) across four generations and 11 TEI-DMGs across five generations. Finally, we estimated the effect size of F0 diet group on F3 and F4 growth and fertility-related phenotypes, providing evidence for transgenerational effects of diet group accompanying inherited differentially methylated genes. Here, for the first time using gene-level and phenotypic data, we demonstrate that a moderate dietary intervention can exert long-lasting transgenerational effects on offspring phenotypes extending beyond the F2 generation in sheep. Full article

The ability of plants to protect themselves from stress-related damages is termed “adaptability” and the phenomenon of showing better performance in subsequent stress is termed “stress memory”. This phenomenon has been reported in various stresses such as drought, heat, salinity, cold, and heavy metal toxicity. Histone modification leading to chromatin remodeling and accumulation of phosphorylated RNA polymerase on the promoters of memory genes is a well-known mechanism of plant stress memory. Recent studies have revealed the role of non-coding RNAs (ncRNAs) and alternative splicing (AS) in memory-specific gene expression and transgenerational inheritance of stress memory. MicroRNAs (miRNAs) inhibit specific genes to enable plants to respond better in subsequent drought and heat stress, while long non-coding RNAs (lncRNAs) play roles in epigenetic regulation of memory gene expression in cold and salt stress. Small interfering RNAs (siRNAs) lead to DNA methylation during the memory response of biotic, salt, and heavy metal stress. Simultaneously, stress-responsive isoforms of tolerant genes are found to be expressed as a memory response in subsequent heat stress. This review highlights the stress-type-specific roles of ncRNAs and AS in establishing, maintaining, and transmitting stress memory, offering insights into their potential for improving crop resilience through genetic and epigenetic priming strategies. Full article

Plants exhibit remarkable adaptability to environmental stresses, with epigenetic modifications playing a key role in stress memory and adaptation. This review explores how epigenetic mechanisms influence hormonal regulation in plants, shaping growth, development, and stress responses. Specifically, we focus on the roles of DNA methylation, histone modifications, and small RNAs in modulating auxin, abscisic acid (ABA), gibberellin (GA), and jasmonic acid (JA) pathways. These pathways influence the plant’s ability to cope with abiotic and biotic stresses and can be inherited by progeny, enhancing stress resilience across generations. By understanding the epigenetic regulation of these hormones, we aim to provide insights into how epigenetic priming can be harnessed in crop improvement to address the challenges posed by climate change. Full article