衰老的分子生物学进展

人们将有机体死亡的可能性随着年龄的增加而增大的现象称为衰老〔1〕。这一定义适用于从酵母到哺乳动物水平的所有生物 ,它表明衰老现象是一个循序渐进的自然过程。同时 ,衰老还表现为某种生物的所有个体随着时间的推移而发生的特征性的表型变化。与疾病衰老 (由疾病引起的生物群体中某些个体的衰老现象 )不同 ,正常衰老影响到种群中的每一个个体 ,是生物体的自然属性。正常衰老和疾病衰老以不同的方式影响生物个体的寿命长短。例如 :由于医药和公共卫生事业的发展 ,疾病引起的衰老得以抑制 ,本世纪发展中国家的人口平均寿命有了大幅度增加 …     

间充质干细胞治疗衰老相关疾病的研究进展

<正>衰老是机体随着年龄增长，器官功能逐步退化的过程，也是生命的自然规律。衰老生物学及衰老相关疾病的干预是当前研究领域亟待解决的难题。干细胞衰老学说认为成体干细胞的衰老枯竭是组织器官衰老及衰老相关疾病的重要诱因，间充质干细胞（MSCs）是一类可在中胚层衍生物（软骨细胞、骨细胞、脂肪细胞）之间分化的成体干细胞亚群，在维持其器官稳态中发挥重要作用，目前已被广泛应用于缓解衰老相关疾病。     

端粒与衰老及特发性肺纤维化的相关性研究

随着老龄化社会的到来,与衰老相关慢性病的发病率呈增长趋势,衰老性疾病已引起国内外多学者的广泛关注。特发性肺纤维化是一种细胞复制性衰老疾病,易受年龄的影响。端粒、端粒酶已被证实为导致衰老的重要机制之一,其在肺部衰老和疾病的发生、发展过程中起着重要作用。进一步研究了解端粒与衰老及特发性肺纤维化的关系,将有助于临床治疗方案的选择,为提高疾病转归提供理论依据。     

自噬调控衰老的研究进展

随着机体老化,组织器官可发生不可逆退行性改变,这些变化与疾病和死亡密切相关。自噬是细胞内一种重要的分解代谢过程,在维持细胞稳态和促进长寿中起重要作用,机体衰老后,其自噬调节能力也随之下降。本文综述了自噬与衰老相关疾病的关系,明确自噬调控衰老的相关分子机制可能为治疗衰老相关疾病提供新的靶点。     

人体心理衰老主要特征和测评方法研究进展

<正>目前衰老与心理学相关的探索正在兴起。有研究提示,保持协调、积极的自我观念有助于成功老龄化和延缓衰老,个体的主观认识和内心体验可影响其行为方式或思想状态,对自身产生正性或负性的影响,延缓或加剧衰老的进程〔1〕。良好的心态有助于延缓衰老、抗衰老。现笔者从人体衰老的心理学角度就心理衰老的概念、特征及影响因素、测评方法的研究动态进行概括。1关于人体心理衰老的概念从目前老年学及医学心理学众多信息分析可知,人体衰老     

线粒体动力学与衰老相关疾病的研究进展

线粒体动力学影响线粒体的形态和功能。随增龄线粒体动力学失衡,导致线粒体功能障碍,加速了老化进展,与衰老相关疾病的发生和发展密切相关,但目前为止,衰老和线粒体动力学之间的具体机制尚不明确。本综述分析了线粒体动力学与衰老的关系,探索了线粒体动力学对衰老相关疾病发生和发展的作用机制,旨在为研发衰老相关疾病的药物提供新的治疗靶...     

衰老相关的T细胞生物学研究进展

T细胞衰老是导致机体衰老、衰老相关疾病以及和寿命直接相关的重要因素。T细胞在免疫系统中处于核心地位 ,参与各种免疫应答 ,执行各种免疫功能 ,抵抗疾病 ,直接或间接地参与细胞免疫和体液免疫。所以 ,研究T细胞衰老是研究人体衰老的重要内容。目前 ,人们在进行衰老生物学研究时 ,常用T细胞作为模型研究基因表达、细胞间通讯及体内平衡调节等 ,其他多细胞生物很少具有T细胞的优点。我们在此主要讨论引起T细胞衰老的因素 (机制 )、由衰老而引起的T细胞功能的相关变化及检测衰老T细胞的常用方法。　　一、引起T细胞衰老的因素　　 1.复制…     

衰老在肺血管疾病中的作用及研究进展

随着我国社会经济的发展以及人口老龄化程度不断加深,衰老相关疾病得到人们越来越多的关注。目前,包括动脉粥样硬化、慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)等在内的众多慢性疾病均证实与衰老密切相关,其具体发病过程和机制也成为研究的热点话题之一。其中,血管在衰老过程中的结构与功能变化是各种老年慢性病发生的重要因素,也是引起机体各器官系统衰老的关键生理病理基础。     

补肾法干预免疫衰老和炎性衰老重建稳态的研究

实现健康的老龄化已是国际性重大公共卫生问题.保持老年人健康是实现积极健康老龄化的关键,也是减轻人口老龄化所带来的社会负担的重要环节.伴随衰老而来的是老年相关疾病如心脑血管疾病、肿瘤、自身免疫性疾病等的高发.开展衰老机制及其干预措施的研究对提高老年人的生活质量、减少医疗费用具有至关重要的意义.揭示衰老机制进而采取有效的干预策略,减少老年疾病的发生,是实现健康老龄化的重要保证.中医药具有丰富有效的延缓衰老的措施,尤其是补肾法在干预衰老(如炎性衰老和免疫衰老)方面具有明显的效果和优势.本文就补肾法重建机体稳态干预免疫衰老和炎性衰老加以综述.     

肾脏衰老机制的探讨

随着科学技术及医学的进步和发展,人口老龄化已成为当今社会面临的重要问题,预计到2030年,≥65岁的老年人口将达到目前人数的2倍,且与年龄相关疾病的发生率将随之升高。由于老龄化与发生肾脏疾病的风险相关,因此研究肾脏衰老相关机制,对于降低老年肾脏病发生率、延缓老年肾脏病发展有重要意义,同时也可减轻家庭、社会经济负担。本文旨在回顾既往发表文献,总结肾脏衰老的可能分子机制。     

Mitochondrial ATP-sensitive potassium channels enhance angiotensin-induced oxidative damage and dopaminergic neuron degeneration. Relevance for aging-associated susceptibility to Parkinson’s disease

Recent studies have shown that renin–angiotensin system overactivation is involved in the aging process in several tissues as well as in longevity and aging-related degenerative diseases by increasing oxidative damage and inflammation. We have recently shown that angiotensin II enhances dopaminergic degeneration by increasing levels of reactive oxygen species and neuroinflammation, and that there is an aging-related increase in angiotensin II activity in the substantia nigra in rats, which may constitute a major factor in the increased risk of Parkinson’s disease with aging. The mechanisms involved in the above mentioned effects and particularly a potential angiotensin–mitochondria interaction have not been clarified. The present study revealed that activation of mitochondrial ATP-sensitive potassium channels [mitoK(ATP)] may play a major role in the angiotensin II-induced effects on aging and neurodegeneration. Inhibition of mitoK(ATP) channels with 5-hydroxydecanoic acid inhibited the increase in dopaminergic cell death induced by angiotensin II, as well as the increase in superoxide/superoxide-derived reactive oxygen species levels and the angiotensin II-induced decrease in the mitochondrial inner membrane potential in cultured dopaminergic neurons. The present study provides data for considering brain renin–angiotensin system and mitoK(ATP) channels as potential targets for protective therapy in aging-associated diseases such as Parkinson’s disease.     

Impact of miRNAs on cardiovascular aging

Aging is a multidimensional process that leads to an increased risk of developing severe diseases, such as cancer and cardiovascular, neurodegenerative, and immunological diseases. Recently, small non-coding RNAs known as microRNAs (miRNAs) have been shown to regulate gene expression, which contributes to many physiological and pathophysiological processes in humans. Increasing evidence suggests that changes in miRNA expression profiles contribute to cellular senescence, aging and aging-related diseases. However, only a few miRNAs whose functions have been elucidated have been associated with aging and/or aging-related diseases. This article reviews the currently available findings regarding the roles of aging-related miRNAs, with a focus on cardiac and cardiovascular aging.     

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??Abstract??Brain aging-related neurological diseases including Alzheimer’s disease and Parkinson’s disease have become one of the major diseases endangering health of older people in our country.Although the mechanism of brain aging and pathogenesis of its related neurodegenerative diseases remain unclear??protein pathological studies such as tau??synuclein and -?amyloid??and researches on functional neuroimaging and biomarkers have now become hot topics in the field of elderly dementia and movement disorders.     

How the effects of aging and stresses of life are integrated in mortality rates: insights for genetic studies of human health and longevity

Increasing proportions of elderly individuals in developed countries combined with substantial increases in related medical expenditures make the improvement of the health of the elderly a high priority today. If the process of aging by individuals is a major cause of age related health declines then postponing aging could be an efficient strategy for improving the health of the elderly. Implementing this strategy requires a better understanding of genetic and non-genetic connections among aging, health, and longevity. We review progress and problems in research areas whose development may contribute to analyses of such connections. These include genetic studies of human aging and longevity, the heterogeneity of populations with respect to their susceptibility to disease and death, forces that shape age patterns of human mortality, secular trends in mortality decline, and integrative mortality modeling using longitudinal data. The dynamic involvement of genetic factors in (i) morbidity/mortality risks, (ii) responses to stresses of life, (iii) multi-morbidities of many elderly individuals, (iv) trade-offs for diseases, (v) genetic heterogeneity, and (vi) other relevant aging-related health declines, underscores the need for a comprehensive, integrated approach to analyze the genetic connections for all of the above aspects of aging-related changes. The dynamic relationships among aging, health, and longevity traits would be better understood if one linked several research fields within one conceptual framework that allowed for efficient analyses of available longitudinal data using the wealth of available knowledge about aging, health, and longevity already accumulated in the research field.     

衰老对心脏结构和功能的影响与机制的研究

衰老是发生在机体内复杂且不可避免的生命现象,导致心脏的结构和功能发生退行性改变,是心血管疾病发生的主要危险因素。因此,了解衰老对心脏的影响及其作用机制,对于预防心血管疾病的发生,提高老年人生活质量具有重要意义。本文将从衰老过程中心脏结构和功能变化、衰老相关心脏疾病以及心脏衰老相关机制方面作简要综述。     

Msh2 promoter region hypermethylation as a marker of aging-related deterioration in old retired female breeder mice

Aging is a process where individuals decrease the performance of their physiological systems and cellular stress response, making them more susceptible to disease and death. The increase in DNA damage associated with age might be recognized as the accumulation of physiological and environmentally induced mutations accompanied with a decline in DNA repair. DNA mismatch repair (MMR) is the main postreplicative correction pathway, which is known to decrease with age. However, since infrequent occurrence of direct DNA damage contrasts with the extensive cell and tissue dysfunction seen in older individuals, the withdrawing of DNA-repairing systems might be also related to epigenetic changes, such as DNA methylation. It has been reported that the physiological stress related to breeding might accelerate the acquisition of aging-related markers; therefore, the aim of this work was to link age with epigenetic modifications in this animal population. Hence, the correlation of Msh2 gene silencing with the deterioration of breeding female mice associated to aging was determined. Combined bisulfite restriction analysis assay was used to compare methylation on DNA isolated from twelve-month-old retired breeders against nulliparous female mice aged-matched, and two-month-old young adults. Our experiments clearly reveal Msh2 promoter hypermethylation associated to the aging process. A higher degree methylation was additionally observed in breeding females DNA. Nevertheless, this additional methylation did not correlate with a further decrease Msh2 mRNA, suggesting that the increase in methylation in old retired breeder might account for further epigenetic changes that could additionally promote the aging process.     

Emerging mitochondrial signaling mechanisms in physiology,aging processes,and as drug targets

Advances in research on mitochondria have elucidated their importance in cell survival and cell death regulation in addition to their function in energy production. Mitochondria are further implicated in various metabolic and aging-related diseases, which are now assumed to be caused by misregulation of physiological systems rather than pure accumulation of oxidative damage. Thus, the signaling mechanisms within mitochondria and between the organelle and its environment have gained interest as potential drug targets. Emerging mitochondrial signaling systems with potential for exploiting them for therapeutic intervention include, among others, the NAD⁺-dependent protein deacetylases of the Sirtuin family, the redox enzyme p66^Shc, and enzymes of the cyclic adenosine monophosphate (cAMP) signaling pathways. Here, we discuss functions of these signaling systems in mitochondria, their roles in aging processes and disease, and their potential to serve as therapeutic targets.     

Birds as long-lived animal models for the study of aging

Despite their high lifetime energy expenditures, most birds can be characterized as long-lived homeotherms with moderately slow aging. A growing body of research confirms the prediction that birds have special adaptations for preventing aging-related oxidative and glycoxidative damage. Nonetheless, biogerontologists have been slow to develop avian laboratory models. A number of domestic poultry and cage bird species represent either established or very promising animal models for studies of basic aging processes and their prevention, including degenerative neurobiological, behavioral and reproductive processes. Several kinds of birds have also been used in studies of cellular resistance to oxidative stressors in vitro. Results of preliminary studies on chickens and quail suggest that caloric restriction may extend the reproductive life span of hens, but its long-term effects on life span remain unstudied. Birds' innate anti-aging mechanisms may actually make them more suitable in some respects as models of longevity than short-lived laboratory rodents, and bird studies may ultimately reveal routes for therapeutic intervention in diseases of human aging and infertility.