Translational Medicine of Aging最新文献

{"title":"Applications of high-throughput ‘omics’ data in the study of frailty","authors":"Wen Lei ,&nbsp;Yudai Xu ,&nbsp;Jun Su ,&nbsp;Cheong-Meng Chong ,&nbsp;Huan-Xing Su ,&nbsp;Junhong Luo ,&nbsp;Evandro F. Fang ,&nbsp;Zhijun Bao ,&nbsp;Guobing Chen","doi":"10.1016/j.tma.2019.04.002","DOIUrl":"10.1016/j.tma.2019.04.002","url":null,"abstract":"<div><p>Frailty is a common geriatric syndrome and a risk factor for many diseases, even mortality. However, the specific molecular biomarkers for diagnosis and therapeutic targets of frailty are still lacking. Studies focusing on molecular profiling in the development of frailty will help address this problem and others. Recently, a series of high-throughput “-omics” technologies have been used to measure thousands of dynamic molecules, including genetic, metabolic, microorganic variables and so on. These omics data extend our understanding of the pathological processes that change with frailty. In this review, we introduce frailty syndrome and summarize current advancements in the applications of omics technologies in the field of frailty.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"3 ","pages":"Pages 40-51"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2019.04.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Steroid signaling mediates longevity responses to the eat-2 genetic model of dietary restriction in Caenorhabditis elegans","authors":"Mindy Farris ,&nbsp;Lily Fang ,&nbsp;Arianne Aslamy ,&nbsp;Victor Pineda","doi":"10.1016/j.tma.2019.09.003","DOIUrl":"10.1016/j.tma.2019.09.003","url":null,"abstract":"<div><p>Dietary restriction (DR) extends lifespan in a wide range of model organisms, including <em>Caenorhabditis elegans</em>. It is an interesting but yet to be addressed question whether hormones serve as a systemic mechanism that mediates this longevity response. We identified a requirement for steroid signaling in lifespan extension induced by DR, by studying two members of the conserved 3β-hydroxysteroid dehydrogenase (3β-HSD) family, HSD-2 and HSD-3. Specifically, we found that lifespan extension in the <em>eat-2</em> genetic model of DR is completely suppressed by a deletion mutant of <em>hsd-2</em>. This suppression is independent of the decreased brood size and prolonged egglay timing of <em>eat-2</em>, as neither was affected by <em>hsd-2</em>, suggesting that the <em>hsd-2</em>-mediated steroid signal regulates longevity without influencing reproduction. Furthermore, <em>hsd-2</em> suppressed the ability of <em>eat-2</em> to resist acute heat shock; stress, as measured by survival after recovery, but only later in life (day 7 and day; 13 adults). This indicates a role for <em>hsd-2</em> in age-dependent responses to DR, consistent with; <em>hsd-2</em> expression, which is primarily in adults. Since <em>hsd-2</em> did not affect DR-induced heat shock resistance in day 1 adults, we hypothesized that <em>hsd-3</em>, which is only expressed in larvae, might be functioning in that role. Indeed, we found that while a deletion mutant of <em>hsd-3</em> does not appear to affect <em>eat-2</em> overall lifespan, it completely suppressed its ability to resist heat shock stress as day 1 adults. Therefore, although both <em>hsd-2</em> and <em>hsd-3</em> contribute to stress resistance in <em>eat-2</em> adults, only <em>hsd-2</em> impacts lifespan, as though steroid signaling in older <em>eat-2</em> adults is more important for lifespan extension than steroid signaling in larvae and young adults. Taken together, our results indicate that steroid signaling through these two steroidogenic enzymes, active at distinct times during the worm lifespan, is vital for the health and longevity conferred by DR.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"3 ","pages":"Pages 90-97"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2019.09.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent studies on anti-aging compounds with Saccharomyces cerevisiae as a model organism","authors":"Gulperi Yalcin,&nbsp;Cheol-Koo Lee","doi":"10.1016/j.tma.2019.10.001","DOIUrl":"10.1016/j.tma.2019.10.001","url":null,"abstract":"<div><p>Extension of lifespan and amelioration of aging-associated phenotypes have been targets of many studies. Some of the established methods of increasing lifespan including dietary restriction and genetic manipulation are difficult to apply to humans, and their side effects are hard to predict. For that reason, it is important to discover compounds that can mimic the anti-aging actions or induce lifespan extension through different metabolisms within the cell. Here we summarize the recent studies to test various types of compounds and materials using budding yeast that show potential anti-aging effects.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"3 ","pages":"Pages 109-115"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2019.10.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rb analog Whi5 regulates G1 to S transition and cell size but not replicative lifespan in budding yeast","authors":"Matthew M. Crane ,&nbsp;Mitsuhiro Tsuchiya ,&nbsp;Ben W. Blue ,&nbsp;Jared D. Almazan ,&nbsp;Kenneth L. Chen ,&nbsp;Siobhan R. Duffy ,&nbsp;Alexandra Golubeva ,&nbsp;Annaiz M. Grimm ,&nbsp;Alison M. Guard ,&nbsp;Shauna A. Hill ,&nbsp;Ellen Huynh ,&nbsp;Ryan M. Kelly ,&nbsp;Michael Kiflezghi ,&nbsp;Hyunsung D. Kim ,&nbsp;Mitchell Lee ,&nbsp;Ting-I. Lee ,&nbsp;Jiayi Li ,&nbsp;Bao M.G. Nguyen ,&nbsp;Riley M. Whalen ,&nbsp;Feng Y. Yeh ,&nbsp;Matt Kaeberlein","doi":"10.1016/j.tma.2019.10.002","DOIUrl":"10.1016/j.tma.2019.10.002","url":null,"abstract":"<div><p>An increase in cell size with age is a characteristic feature of replicative aging in budding yeast. Deletion of the gene encoding Whi5 results in shortened duration of G1 and reduced cell size, and has been previously suggested to increase replicative lifespan. Upon careful analysis of multiple independently derived haploid and homozygous diploid <em>whi5Δ</em> mutants, we find no effect on lifespan, but we do confirm the reduction in cell size. We suggest that instead of antagonizing lifespan, the elongated G1 phase of the cell cycle during aging may actually play an important role in allowing aged cells time to repair accumulating DNA damage.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"3 ","pages":"Pages 104-108"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2019.10.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10076545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Senescence in aging and disorders of the central nervous system","authors":"Barbara L. Swenson ,&nbsp;Charlton F. Meyer ,&nbsp;Tyler J. Bussian ,&nbsp;Darren J. Baker","doi":"10.1016/j.tma.2019.01.002","DOIUrl":"10.1016/j.tma.2019.01.002","url":null,"abstract":"<div><p>Aging can be defined as the natural process of accumulating time during the life of an organism. Advancing age correlates with tissue dysfunction, including frailty, malignancies, immobility, and cognitive loss. With increasing age, there is an accumulation of cells that have lost their ability to divide and yet do not undergo cell death, termed senescent cells. These cells, which are characterized by a distinctive proinflammatory phenotype, have been demonstrated to damage surrounding cells, which negatively impact health. Within the brain, senescent cells have been associated with a variety of diseases, including Parkinson’s and Alzheimer’s disease, and maladies where chronic inflammation drives tissue deterioration. Here, we describe the resident cells of the central nervous system (CNS), how they exhibit tendencies toward senescence with age and disease, and discuss tools that will be useful to aid in senescent cell identification and characterization in this tissue.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"3 ","pages":"Pages 17-25"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2019.01.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent progresses on anti-aging compounds and their targets in Caenorhabditis elegans","authors":"Eun Ji E. Kim,&nbsp;Seung-Jae V. Lee","doi":"10.1016/j.tma.2019.11.003","DOIUrl":"10.1016/j.tma.2019.11.003","url":null,"abstract":"<div><p>Searching for drugs that extend healthy lifespan and the subsequent analysis of their mechanisms of action is a crucial aspect for aging research. However, identifying both longevity-enhancing drugs and their corresponding targets is challenging. The roundworm <em>Caenorhabditis elegans</em> is a suitable model for such research because of its short lifespan and genetic tractability. In this perspective, we discuss recent progresses on the identification of anti-aging drugs and characterization of their targets using <em>C. elegans</em> as a model organism. In particular, minocycline, JZL184, monorden, and paxilline increase <em>C. elegans</em> lifespan by inhibiting 18S rRNA/ribosome, fatty acid amide hydrolase-4, Hsp90, and the Ca²⁺-activated K⁺ (BK) channel SLO-1, respectively. Because many factors that regulate aging and lifespan in <em>C. elegans</em> are evolutionarily conserved, these newly identified lifespan-extending compounds may guide the development of anti-aging medicines for humans.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"3 ","pages":"Pages 121-124"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2019.11.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of the circadian clock in fine-tuning the process of leaf senescence in plants","authors":"Hyunmin Kim,&nbsp;Sunghyun Hong","doi":"10.1016/j.tma.2018.12.001","DOIUrl":"10.1016/j.tma.2018.12.001","url":null,"abstract":"<div><p>Leaf senescence is a developmental process and a critical evolutionary strategy for fitness in plants, involving highly organized regulatory mechanisms. Many environmental signals as well as internal developmental aging trigger leaf senescence. Circadian clocks provide timing information for the adaptation of organisms to changing environmental conditions via dynamic metabolic and physiological regulatory networks. Interactions between aging and the circadian clock have been well characterized in animals. In plants, recent studies reveal similar interactions between leaf senescence and the circadian clock, supporting the evolutionary conservation of these interactions in both animal and plant kingdoms. In this review, we discuss the major clock components and senescence regulators that connect these two regulatory mechanisms, and the significance of this relationship in the plant life history.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"3 ","pages":"Pages 26-30"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2018.12.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gene network analysis of senescence-associated genes in annual plants and comparative assessment of aging in perennials and animals","authors":"Hou-Ling Wang ,&nbsp;Hongwei Guo ,&nbsp;Zhonghai Li","doi":"10.1016/j.tma.2018.12.003","DOIUrl":"10.1016/j.tma.2018.12.003","url":null,"abstract":"<div><p>Aging, resulting from degenerative changes in cell metabolism, affects fecundity and longevity. To increase lifespan in animals or plants, manipulation in gene modification or pharmacology intervention has been proved to be as feasible approaches. NAD⁺, spermidine, and rapamycin, as well as genetic editing, bring to light at the tunnel end for the longevity in animals. In plants, the existing evidence suggests that they may share common aging signaling pathway with animals. However, as sessile organisms, plants got to cope with complex environmental changes and evolved specific signaling pathways. Here, we reviewed the latest research advances in plant aging to make a gene network analysis of senescence-associated genes in annual plant and perform a comparative assessment of aging in perennials as well as animals.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"3 ","pages":"Pages 6-13"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2018.12.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amino acids in the regulation of aging and aging-related diseases","authors":"Clare-Ann Canfield ,&nbsp;Patrick C. Bradshaw","doi":"10.1016/j.tma.2019.09.001","DOIUrl":"10.1016/j.tma.2019.09.001","url":null,"abstract":"<div><p>Amino acids are the building blocks of protein, but also play important cellular signaling roles. The mechanisms through which altered levels of many amino acids are sensed and the signals transmitted are still largely unknown. Increasing evidence is showing that these signals may influence the aging process. In this regard, methionine restriction appears to be an evolutionary conserved mechanism to delay aging and supplementation with glycine can mimic methionine restriction to extend lifespan in rodents. Tryptophan restriction may also activate specific anti-aging pathways, but it could interfere with cognitive function. With exercise the consumption of dietary branched chain amino acids (BCAAs) may be beneficial in building muscle mass, but high levels of BCAAs as well as tyrosine and phenylalanine in the bloodstream are associated with metabolic disease such as insulin resistance. Individual supplementation or restriction of several different amino acids has shown promise in the treatment of insulin resistance in rodents. Much progress regarding the effects of amino acids on longevity has been made using yeast, nematodes, and fruit flies. Clearly, much more research is needed to understand the signaling pathways activated by amino acid imbalance before efficacious and well-tolerated dietary interventions can be developed for human aging and aging-related disorders. In this review the mechanisms through which altered dietary and cellular levels of the twenty proteogenic amino acids affect aging or aging-related disorders are discussed.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"3 ","pages":"Pages 70-89"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2019.09.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in pharmacological interventions of aging in mice","authors":"Minxian Qian ,&nbsp;Baohua Liu","doi":"10.1016/j.tma.2019.11.002","DOIUrl":"10.1016/j.tma.2019.11.002","url":null,"abstract":"<div><p>The remarkable breakthroughs in aging research pave the way allowing us to explore potential interventions to slow down aging process, and more importantly, to improve healthiness. Multiple approaches, including pharmacological and non-pharmacological interventions (e.g. caloric restriction, physical exercise), to a great extent, successfully tackle challenges of age-related phenotypic deficits across species. To date, molecular compounds are largely emerging, such as caloric restriction mimetics, NAD⁺ boosters, and senolytics. The use of mouse models is essential, as one of the best tools, to evaluate the potentials of molecules against aging and to provide a translational basis for treating human frailty. Here, we briefly overview present advances on therapeutic interventions against aging in laboratory mouse models and discuss the benefits and pitfalls on their clinical application for anti-aging and aging-related pathologies in humans.</p></div>","PeriodicalId":36555,"journal":{"name":"Translational Medicine of Aging","volume":"3 ","pages":"Pages 116-120"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tma.2019.11.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55175674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}