Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, Год журнала: 2011, Номер 714(1-2), С. 105 - 112
Опубликована: Май 21, 2011
Язык: Английский
Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis, Год журнала: 2011, Номер 714(1-2), С. 105 - 112
Опубликована: Май 21, 2011
Язык: Английский
Genome Biology, Год журнала: 2015, Номер 16(1)
Опубликована: Янв. 29, 2015
Abstract Background DNA methylation levels change with age. Recent studies have identified biomarkers of chronological age based on levels. It is not yet known whether captures aspects biological Results Here we test differences between people’s ages and estimated ages, age, predict all-cause mortality in later life. The difference (Δ ) was calculated four longitudinal cohorts older people. Meta-analysis proportional hazards models from the used to determine association Δ mortality. A 5-year higher associated a 21% risk, adjusting for sex. After further adjustments childhood IQ, education, social class, hypertension, diabetes, cardiovascular disease, APOE e4 status, there 16% increased risk those . pedigree-based heritability analysis conducted separate cohort. 0.43. Conclusions methylation-derived measures accelerated aging are heritable traits that independently health lifestyle factors, genetic factors.
Язык: Английский
Процитировано
1120International Journal of Epidemiology, Год журнала: 2011, Номер 41(1), С. 79 - 105
Опубликована: Дек. 13, 2011
Every year more than 13 million deaths worldwide are due to environmental pollutants, and approximately 24% of diseases caused by exposures that might be averted through preventive measures. Rapidly growing evidence has linked pollutants with epigenetic variations, including changes in DNA methylation, histone modifications microRNAs. Environ mental chemicals All these mechanisms likely play important roles disease aetiology, their provide further understanding as well biomarkers reflecting and/or predicting the risk future disease. We summarize findings on alterations related chemical exposures, propose action means which may cause such changes. discuss opportunities, challenges directions for epidemiology research epigenomics. Future investigations needed solve methodological practical challenges, uncertainties about stability over time epigenomic induced environment, tissue specificity alterations, validation laboratory methods, adaptation bioinformatic biostatistical methods high-throughput In addition, there numerous reports arising following exposure toxicants, but most have not been directly endpoints. To complete our discussion, we also briefly chemicals-related
Язык: Английский
Процитировано
433International Journal of Molecular Sciences, Год журнала: 2018, Номер 19(10), С. 2937 - 2937
Опубликована: Сен. 27, 2018
Ageing is a major risk factor for developing many neurodegenerative diseases. Cellular senescence homeostatic biological process that has key role in driving ageing. There evidence senescent cells accumulate the nervous system with ageing and disease may predispose person to appearance of condition or aggravate its course. Research into long been hindered by variable cell-type specific features lack universal marker unequivocally detect cells. Recent advances markers genetically modified animal models have boosted our knowledge on cellular age-related disease. The aim now fully elucidate neurodegeneration order efficiently safely exploit as therapeutic target. Here, we review neurons glial discuss putative Alzheimer's disease, Parkinson's multiple sclerosis provide, first time, glia sclerosis, using novel GL13 lipofuscin stain senescence.
Язык: Английский
Процитировано
351Acta Physiologica, Год журнала: 2011, Номер 202(2), С. 103 - 118
Опубликована: Март 14, 2011
Dietary exposures can have consequences for health years or decades later and this raises questions about the mechanisms through which such are 'remembered' how they result in altered disease risk. There is growing evidence that epigenetic may mediate effects of nutrition be causal development common complex (or chronic) diseases. Epigenetics encompasses changes to marks on genome (and associated cellular machinery) copied from one cell generation next, alter gene expression, but do not involve primary DNA sequence. These include three distinct, closely inter-acting, including methylation, histone modifications non-coding microRNAs (miRNA) which, together, responsible regulating expression only during differentiation embryonic foetal also throughout life-course. This review summarizes numerous dietary factors, micronutrients non-nutrient components as genistein polyphenols, modify marks. In some cases, example, supply methyl donors there plausible explanations observed changes, a large extent, diet–epigenome–health relationships remain discovered. addition, relatively little known epigenomic most labile response exposures. Given plasticity their responsiveness potential biomarkers use intervention studies.
Язык: Английский
Процитировано
318ILAR Journal, Год журнала: 2012, Номер 53(3-4), С. 289 - 305
Опубликована: Дек. 1, 2012
This review focuses on how environmental factors through epigenetics modify disease risk and health outcomes. Major epigenetic events, such as histone modifications, DNA methylation, microRNA expression, are described. The function of dose, duration, composition, window exposure in remodeling the individual's terrain susceptibility addressed. ideas lifelong editing early-life memories, transgenerational effects germline transmission, potential role hydroxylmethylation cytosine developmental reprogramming discussed. Finally, several major classes reviewed context pathogenesis disease. These include endocrine disruptors, tobacco smoke, polycyclic aromatic hydrocarbons, infectious pathogens, particulate matter, diesel exhaust particles, dust mites, fungi, heavy metals, other indoor outdoor pollutants. We conclude that summation modifications induced by multiple exposures, accumulated over time, represented broad or narrow, acute chronic, lifelong, may provide a more precise assessment consequences. Future investigations focus their use readouts biomarkers totality past for prediction future prescription effective countermeasures.
Язык: Английский
Процитировано
254The Annual Review of Pharmacology and Toxicology, Год журнала: 2011, Номер 52(1), С. 37 - 56
Опубликована: Март 3, 2011
Xenobiotics are encountered by humans on a daily basis and include drugs, environmental pollutants, cosmetics, even components of the diet. These chemicals undergo metabolism detoxication to produce numerous metabolites, some which have potential cause unintended effects such as toxicity. They can also block action enzymes or receptors used for endogenous affect efficacy and/or bioavailability coadministered drug. Therefore, it is essential determine full metabolic that these body. Metabolomics, comprehensive analysis small molecules in biofluid, reveal biologically relevant perturbations result from xenobiotic exposure. This review discusses impact genetic, environmental, gut microflora variation has metabolome, how variables may interact, positively negatively, with metabolism.
Язык: Английский
Процитировано
248Methods in molecular biology, Год журнала: 2014, Номер unknown, С. 3 - 25
Опубликована: Ноя. 8, 2014
Язык: Английский
Процитировано
231Current Opinion in Rheumatology, Год журнала: 2016, Номер 28(5), С. 497 - 505
Опубликована: Июль 14, 2016
Purpose of review This examines evidence relating environmental factors to the development systemic lupus erythematosus (SLE). Recent findings The strongest epidemiologic exists for associations silica, cigarette smoking, oral contraceptives, postmenopausal hormone therapy and endometriosis, with SLE incidence. studies have also provided robust association between alcohol consumption decreased risk. There are preliminary, conflicting or unsubstantiated data that other factors, including air pollution, ultraviolet light, infections, vaccinations, solvents, pesticides heavy metals such as mercury, related Biologic mechanisms linking exposures risk include increased oxidative stress, inflammation inflammatory cytokine upregulation, hormonal triggers, well epigenetic modifications resulting from exposure could lead SLE. Summary Identifying is essential it will understanding pathogenesis this complex disease make factor modification possible those at
Язык: Английский
Процитировано
220Frontiers in Molecular Neuroscience, Год журнала: 2018, Номер 11
Опубликована: Сен. 28, 2018
Parents' stressful experiences can influence an offspring's vulnerability to many pathological conditions, including psychopathologies, and their effects may even endure for several generations. Nevertheless, the cause of this phenomenon has not been determined, only recently have scientists turned epigenetics answer question. There is extensive literature on epigenetics, but no consensus exists with regard how what (and must) be considered study define processes inheritance. In work, we aimed clarify systematize these concepts. To end, analyzed dynamics epigenetic changes over time in detail defined three types epigenetics: a direct form (DE) two indirect processes-within (WIE) across (AIE). DE refers that occur lifespan individual, due his environment. WIE concerns inside womb, events during gestation. Finally, AIE defines affect individual's predecessors (parents, grandparents, etc.), long before conception are somehow (e.g., through gametes, intrauterine environment setting) transmitted This distinction allows us organize main body evidence according categories then focus latter (AIE), referring it as faster route informational transmission generations-compared genetic inheritance-that guides human evolution Lamarckian (i.e., experience-dependent) manner. Of molecular implicated phenomenon, well-known (methylation) novel (non-coding RNA, ncRNA) regulatory mechanisms converging. Our discussion chief methods used inheritance highlights most compelling technical theoretical problems discipline. Experimental suggestions expand field provided, practical ethical implications discussed extensively.
Язык: Английский
Процитировано
219Molecular Genetics and Metabolism, Год журнала: 2013, Номер 110(1-2), С. 25 - 34
Опубликована: Июль 19, 2013
Язык: Английский
Процитировано
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