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    1449 results match your criteria Aging Cell [Journal]

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    17α-estradiol acts through hypothalamic pro-opiomelanocortin expressing neurons to reduce feeding behavior.
    Aging Cell 2017 Nov 23. Epub 2017 Nov 23.
    Department of Nutritional Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
    Weight loss is an effective intervention for diminishing disease burden in obese older adults. Pharmacological interventions that reduce food intake and thereby promote weight loss may offer effective strategies to reduce age-related disease. We previously reported that 17α-estradiol (17α-E2) administration elicits beneficial effects on metabolism and inflammation in old male mice. Read More

    Comparative proteomic profiling reveals a role for Cisd2 in skeletal muscle aging.
    Aging Cell 2017 Nov 23. Epub 2017 Nov 23.
    Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei, Taiwan.
    Skeletal muscle has emerged as one of the most important tissues involved in regulating systemic metabolism. The gastrocnemius is a powerful skeletal muscle composed of predominantly glycolytic fast-twitch fibers that are preferentially lost among old age. This decrease in gastrocnemius muscle mass is remarkable during aging; however, the underlying molecular mechanism is not fully understood. Read More

    DLP1-dependent mitochondrial fragmentation and redistribution mediate prion-associated mitochondrial dysfunction and neuronal death.
    Aging Cell 2017 Nov 22. Epub 2017 Nov 22.
    National Animal Transmissible Spongiform Encephalopathy Laboratory, State Key Laboratories for Agrobiotechnology, Key Laboratory of Animal Epidemiology and Zoonosis, College of Veterinary Medicine, Ministry of Agriculture, China Agricultural University, Beijing, 100193, China.
    Mitochondrial malfunction is a universal and critical step in the pathogenesis of many neurodegenerative diseases including prion diseases. Dynamin-like protein 1 (DLP1) is one of the key regulators of mitochondrial fission. In this study, we investigated the role of DLP1 in mitochondrial fragmentation and dysfunction in neurons using in vitro and in vivo prion disease models. Read More

    Cellular aging dynamics after acute malaria infection: A 12-month longitudinal study.
    Aging Cell 2017 Nov 16. Epub 2017 Nov 16.
    Unit of Infectious Diseases, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Accelerated cellular aging and reduced lifespan have recently been shown in birds chronically infected with malaria parasites. Whether malaria infection also affects cellular aging in humans has not been reported. Here, we assessed the effect of a single acute Plasmodium falciparum malaria infection on cellular aging dynamics in travelers prospectively followed over one year in Sweden. Read More

    SIRT3 deregulation is linked to mitochondrial dysfunction in Alzheimer's disease.
    Aging Cell 2017 Nov 11. Epub 2017 Nov 11.
    VA Boston Healthcare System, Boston, MA, 02130, USA.
    Alzheimer's disease (AD) is the leading cause of dementia in the elderly. Despite decades of study, effective treatments for AD are lacking. Mitochondrial dysfunction has been closely linked to the pathogenesis of AD, but the relationship between mitochondrial pathology and neuronal damage is poorly understood. Read More

    Running-wheel activity delays mitochondrial respiratory flux decline in aging mouse muscle via a post-transcriptional mechanism.
    Aging Cell 2017 Nov 9. Epub 2017 Nov 9.
    Section Systems Medicine of Metabolism and Signaling, Laboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
    Loss of mitochondrial respiratory flux is a hallmark of skeletal muscle aging, contributing to a progressive decline of muscle strength. Endurance exercise alleviates the decrease in respiratory flux, both in humans and in rodents. Here, we dissect the underlying mechanism of mitochondrial flux decline by integrated analysis of the molecular network. Read More

    Ketone body 3-hydroxybutyrate mimics calorie restriction via the Nrf2 activator, fumarate, in the retina.
    Aging Cell 2017 Nov 9. Epub 2017 Nov 9.
    Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
    Calorie restriction (CR) being the most robust dietary intervention provides various health benefits. D-3-hydroxybutyrate (3HB), a major physiological ketone, has been proposed as an important endogenous molecule for CR. To investigate the role of 3HB in CR, we investigated potential shared mechanisms underlying increased retinal 3HB induced by CR and exogenously applied 3HB without CR to protect against ischemic retinal degeneration. Read More

    Brain 5-lipoxygenase over-expression worsens memory, synaptic integrity, and tau pathology in the P301S mice.
    Aging Cell 2017 Nov 4. Epub 2017 Nov 4.
    Department of Pharmacology, Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.
    Progressive accumulation of highly phosphorylated tau protein isoforms is the main feature of a group of neurodegenerative diseases collectively called tauopathies. Data from human and animal models of these diseases have shown that neuroinflammation often accompanies their pathogenesis. The 5-lipoxygenase (5LO) is an enzyme widely expressed in the brain and a source of potent pro-inflammatory mediators, while its pharmacological inhibition modulates the phenotype of a tau transgenic mouse model, the htau mice. Read More

    Amyloid Beta monomers regulate cyclic adenosine monophosphate response element binding protein functions by activating type-1 insulin-like growth factor receptors in neuronal cells.
    Aging Cell 2017 Nov 1. Epub 2017 Nov 1.
    Institute of Biostructures and Bioimaging, National Council of Research (IBB-CNR), Via Paolo Gaifami 18, 95126, Catania, Italy.
    Alzheimer's disease (AD) is a progressive neurodegenerative disorder associated with synaptic dysfunction, pathological accumulation of β-amyloid (Aβ), and neuronal loss. The self-association of Aβ monomers into soluble oligomers seems to be crucial for the development of neurotoxicity (J. Neurochem. Read More

    Sirt2-BubR1 acetylation pathway mediates the effects of advanced maternal age on oocyte quality.
    Aging Cell 2017 Oct 25. Epub 2017 Oct 25.
    State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.
    The level of Sirt2 protein is reduced in oocytes from aged mice, while exogenous expression of Sirt2 could ameliorate the maternal age-associated meiotic defects. To date, the underlying mechanism remains unclear. Here, we confirmed that specific depletion of Sirt2 disrupts maturational progression and spindle/chromosome organization in mouse oocytes, with compromised kinetochore-microtubule attachments. Read More

    PGC-1α affects aging-related changes in muscle and motor function by modulating specific exercise-mediated changes in old mice.
    Aging Cell 2017 Oct 25. Epub 2017 Oct 25.
    Biozentrum, University of Basel, Basel, Switzerland.
    The age-related impairment in muscle function results in a drastic decline in motor coordination and mobility in elderly individuals. Regular physical activity is the only efficient intervention to prevent and treat this age-associated degeneration. However, the mechanisms that underlie the therapeutic effect of exercise in this context remain unclear. Read More

    Enhanced inflammation and attenuated tumor suppressor pathways are associated with oncogene-induced lung tumors in aged mice.
    Aging Cell 2017 Oct 18. Epub 2017 Oct 18.
    Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA.
    Aging is often accompanied by a dramatic increase in cancer susceptibility. To gain insights into how aging affects tumor susceptibility, we generated a conditional mouse model in which oncogenic Kras(G12D) was activated specifically in lungs of young (3-5 months) and old (19-24 months) mice. Activation of Kras(G12D) in old mice resulted in shorter survival and development of higher-grade lung tumors. Read More

    Influence of cell distribution and diabetes status on the association between mitochondrial DNA copy number and aging phenotypes in the InCHIANTI study.
    Aging Cell 2017 Oct 19. Epub 2017 Oct 19.
    Longitudinal Studies Section, Translational Gerontology Branch, National Institute on Aging, Baltimore, MD, USA.
    Mitochondrial DNA copy number (mtDNA-CN) estimated in whole blood is a novel marker of mitochondrial mass and function that can be used in large population-based studies. Analyses that attempt to relate mtDNA-CN to specific aging phenotypes may be confounded by differences in the distribution of blood cell types across samples. Also, low or high mtDNA-CN may have a different meaning given the presence of diseases associated with mitochondrial damage. Read More

    Anti-inflammaging effects of human alpha-1 antitrypsin.
    Aging Cell 2017 Oct 17. Epub 2017 Oct 17.
    Department of Molecular Genetics & Microbiology, University of Florida, Gainesville, FL, USA.
    Inflammaging plays an important role in most age-related diseases. However, the mechanism of inflammaging is largely unknown, and therapeutic control of inflammaging is challenging. Human alpha-1 antitrypsin (hAAT) has immune-regulatory, anti-inflammatory, and cytoprotective properties as demonstrated in several disease models including type 1 diabetes, arthritis, lupus, osteoporosis, and stroke. Read More

    Age-associated microRNA expression in human peripheral blood is associated with all-cause mortality and age-related traits.
    Aging Cell 2017 Oct 17. Epub 2017 Oct 17.
    The Framingham Heart Study, Framingham, MA, USA.
    Recent studies provide evidence of correlations of DNA methylation and expression of protein-coding genes with human aging. The relations of microRNA expression with age and age-related clinical outcomes have not been characterized thoroughly. We explored associations of age with whole-blood microRNA expression in 5221 adults and identified 127 microRNAs that were differentially expressed by age at P < 3. Read More

    Human CD8(+) EMRA T cells display a senescence-associated secretory phenotype regulated by p38 MAPK.
    Aging Cell 2017 Oct 12. Epub 2017 Oct 12.
    Translational Medicine and Therapeutics, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
    Cellular senescence is accompanied by a senescence-associated secretory phenotype (SASP). We show here that primary human senescent CD8(+) T cells also display a SASP comprising chemokines, cytokines and extracellular matrix remodelling proteases that are unique to this subset and contribute to age-associated inflammation. We found the CD8(+) CD45RA(+) CD27(-) EMRA subset to be the most heterogeneous, with a population aligning with the naïve T cells and another with a closer association to the effector memory subset. Read More

    Ghrelin deletion protects against age-associated hepatic steatosis by downregulating the C/EBPα-p300/DGAT1 pathway.
    Aging Cell 2017 Oct 12. Epub 2017 Oct 12.
    Department of Medicine, Baylor College of Medicine, Division of Endocrinology, Diabetes and Metabolism, MCL, Center for Translational Research in Inflammatory Diseases, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, 77030, USA.
    Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide. NAFLD usually begins as low-grade hepatic steatosis which further progresses in an age-dependent manner to nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma in some patients. Ghrelin is a hormone known to promote adiposity in rodents and humans, but its potential role in hepatic steatosis is unknown. Read More

    In vivo properties of the disaggregase function of J-proteins and Hsc70 in Caenorhabditis elegans stress and aging.
    Aging Cell 2017 Dec 10;16(6):1414-1424. Epub 2017 Oct 10.
    Center for Molecular Biology (ZMBH), Heidelberg University, 69120, Heidelberg, Germany.
    Protein aggregation is enhanced upon exposure to various stress conditions and aging, which suggests that the quality control machinery regulating protein homeostasis could exhibit varied capacities in different stages of organismal lifespan. Recently, an efficient metazoan disaggregase activity was identified in vitro, which requires the Hsp70 chaperone and Hsp110 nucleotide exchange factor, together with single or cooperating J-protein co-chaperones of classes A and B. Here, we describe how the orthologous Hsp70s and J-protein of Caenorhabditis elegans work together to resolve protein aggregates both in vivo and in vitro to benefit organismal health. Read More

    Interplay of pathogenic forms of human tau with different autophagic pathways.
    Aging Cell 2017 Oct 12. Epub 2017 Oct 12.
    Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY, 10461, USA.
    Loss of neuronal proteostasis, a common feature of the aging brain, is accelerated in neurodegenerative disorders, including different types of tauopathies. Aberrant turnover of tau, a microtubule-stabilizing protein, contributes to its accumulation and subsequent toxicity in tauopathy patients' brains. A direct toxic effect of pathogenic forms of tau on the proteolytic systems that normally contribute to their turnover has been proposed. Read More

    Age-associated dysregulation of protein metabolism in the mammalian oocyte.
    Aging Cell 2017 Dec 10;16(6):1381-1393. Epub 2017 Oct 10.
    Stowers Institute for Medical Research, Kansas City, MO, 64110, USA.
    Reproductive aging is characterized by a marked decline in oocyte quality that contributes to infertility, miscarriages, and birth defects. This decline is multifactorial, and the underlying mechanisms are under active investigation. Here, we performed RNA-Seq on individual growing follicles from reproductively young and old mice to identify age-dependent functions in oocytes. Read More

    Sirtuins at the crossroads of stemness, aging, and cancer.
    Aging Cell 2017 Dec 10;16(6):1208-1218. Epub 2017 Oct 10.
    Laboratory for Molecular Cancer Biology, Department of Radiation Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
    Sirtuins are stress-responsive proteins that direct various post-translational modifications (PTMs) and as a result, are considered to be master regulators of several cellular processes. They are known to both extend lifespan and regulate spontaneous tumor development. As both aging and cancer are associated with altered stem cell function, the possibility that the involvement of sirtuins in these events is mediated by their roles in stem cells is worthy of investigation. Read More

    Loss of SIRT2 leads to axonal degeneration and locomotor disability associated with redox and energy imbalance.
    Aging Cell 2017 Dec 5;16(6):1404-1413. Epub 2017 Oct 5.
    Neurometabolic Diseases Laboratory, Institute of Neuropathology, IDIBELL, Barcelona, Spain.
    Sirtuin 2 (SIRT2) is a member of a family of NAD(+) -dependent histone deacetylases (HDAC) that play diverse roles in cellular metabolism and especially for aging process. SIRT2 is located in the nucleus, cytoplasm, and mitochondria, is highly expressed in the central nervous system (CNS), and has been reported to regulate a variety of processes including oxidative stress, genome integrity, and myelination. However, little is known about the role of SIRT2 in the nervous system specifically during aging. Read More

    Dopamine D4 receptor activation restores CA1 LTP in hippocampal slices from aged mice.
    Aging Cell 2017 Dec 3;16(6):1323-1333. Epub 2017 Oct 3.
    Key Lab of Brain Research of Henan Province, Department of Physiology and Neurobiology, Xinxiang Medical University, Xinxiang, China.
    Normal aging is characterized with a decline in hippocampal memory functions that is associated with changes in long-term potentiation (LTP) of the CA3-to-CA1 synapse. Age-related deficit of the dopaminergic system may contribute to impairment of CA1 LTP. Here we assessed how the modulation of CA1 LTP by dopamine is affected by aging and how it is dependent on the Ca(2+) source. Read More

    TOR-mediated regulation of metabolism in aging.
    Aging Cell 2017 Dec 2;16(6):1219-1233. Epub 2017 Oct 2.
    Federated Department of Biological Sciences, New Jersey Institute of Technology, Rutgers University, Newark, NJ, 07102, USA.
    Cellular metabolism is regulated by the mTOR kinase, a key component of the molecular nutrient sensor pathway that plays a central role in cellular survival and aging. The mTOR pathway promotes protein and lipid synthesis and inhibits autophagy, a process known for its contribution to longevity in several model organisms. The nutrient-sensing pathway is regulated at the lysosomal membrane by a number of proteins for which deficiency triggers widespread aging phenotypes in tested animal models. Read More

    miR-155 induces ROS generation through downregulation of antioxidation-related genes in mesenchymal stem cells.
    Aging Cell 2017 Dec 2;16(6):1369-1380. Epub 2017 Oct 2.
    Division of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
    Inflammation-induced reactive oxygen species (ROS) are implicated in cellular dysfunction and an important trigger for aging- or disease-related tissue degeneration. Inflammation-induced ROS in stem cells lead to deterioration of their properties, altering tissue renewal or regeneration. Pathological ROS generation can be induced by multiple steps, and dysfunction of antioxidant systems is a major cause. Read More

    MicroRNAs mir-184 and let-7 alter Drosophila metabolism and longevity.
    Aging Cell 2017 Dec 29;16(6):1434-1438. Epub 2017 Sep 29.
    Department of Molecular and Integrative Physiology and the Geriatrics Center, University of Michigan, Ann Arbor, Michigan, 48109, USA.
    MicroRNAs (miRNAs) are small RNA molecules that regulate gene expression associated with many complex biological processes. By comparing miRNA expression between long-lived cohorts of Drosophila melanogaster that were fed a low-nutrient diet with normal-lived control animals fed a high-nutrient diet, we identified miR-184, let-7, miR-125, and miR-100 as candidate miRNAs involved in modulating aging. We found that ubiquitous, adult-specific overexpression of these individual miRNAs led to significant changes in fat metabolism and/or lifespan. Read More

    Caloric restriction stabilizes body weight and accelerates behavioral recovery in aged rats after focal ischemia.
    Aging Cell 2017 Dec 29;16(6):1394-1403. Epub 2017 Sep 29.
    University of Medicine and Pharmacy Craiova, Neurobiology of Aging Group, Craiova, Romania.
    Obesity and hyperinsulinemia are risk factors for stroke. We tested the hypothesis that caloric restriction, which reduces the incidence of age-related obesity and metabolic syndrome, may represent an efficient and cost-effective strategy for preventing stroke and its devastating consequences. To this end, we placed aged, obese Sprague-Dawley aged rats on a calorie-restricted diet for 8 weeks prior to the experimental infarction. Read More

    Sexually divergent DNA methylation patterns with hippocampal aging.
    Aging Cell 2017 Dec 25;16(6):1342-1352. Epub 2017 Sep 25.
    Reynolds Oklahoma Center on Aging, Oklahoma, OK, USA.
    DNA methylation is a central regulator of genome function, and altered methylation patterns are indicative of biological aging and mortality. Age-related cellular, biochemical, and molecular changes in the hippocampus lead to cognitive impairments and greater vulnerability to neurodegenerative disease that varies between the sexes. The role of hippocampal epigenomic changes with aging in these processes is unknown as no genome-wide analyses of age-related methylation changes have considered the factor of sex in a controlled animal model. Read More

    Gene therapy with the TRF1 telomere gene rescues decreased TRF1 levels with aging and prolongs mouse health span.
    Aging Cell 2017 Dec 24;16(6):1353-1368. Epub 2017 Sep 24.
    Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Centre (CNIO), Melchor Fernández Almagro 3, Madrid, E-28029, Spain.
    The shelterin complex protects telomeres by preventing them from being degraded and recognized as double-strand DNA breaks. TRF1 is an essential component of shelterin, with important roles in telomere protection and telomere replication. We previously showed that TRF1 deficiency in the context of different mouse tissues leads to loss of tissue homeostasis owing to impaired stem cell function. Read More

    Transthyretin deposition promotes progression of osteoarthritis.
    Aging Cell 2017 Dec 22;16(6):1313-1322. Epub 2017 Sep 22.
    Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, USA.
    Deposition of amyloid is a common aging-associated phenomenon in several aging-related diseases. Osteoarthritis (OA) is the most prevalent joint disease, and aging is its major risk factor. Transthyretin (TTR) is an amyloidogenic protein that is deposited in aging and OA-affected human cartilage and promotes inflammatory and catabolic responses in cultured chondrocytes. Read More

    Genetic interaction with temperature is an important determinant of nematode longevity.
    Aging Cell 2017 Dec 21;16(6):1425-1429. Epub 2017 Sep 21.
    Cellular and Molecular Biology Program, University of Michigan, Ann Arbor, MI, 48109, USA.
    As in other poikilotherms, longevity in C. elegans varies inversely with temperature; worms are longer-lived at lower temperatures. While this observation may seem intuitive based on thermodynamics, the molecular and genetic basis for this phenomenon is not well understood. Read More

    In a randomized trial in prostate cancer patients, dietary protein restriction modifies markers of leptin and insulin signaling in plasma extracellular vesicles.
    Aging Cell 2017 Dec 17;16(6):1430-1433. Epub 2017 Sep 17.
    Division of Geriatrics and Nutritional Sciences and Center for Human Nutrition, Washington University School of Medicine, St. Louis, MO, 63110, USA.
    Obesity, metabolic syndrome, and hyperleptinemia are associated with aging and age-associated diseases including prostate cancer. One experimental approach to inhibit tumor growth is to reduce dietary protein intake and hence levels of circulating amino acids. Dietary protein restriction (PR) increases insulin sensitivity and suppresses prostate cancer cell tumor growth in animal models, providing a rationale for clinical trials. Read More

    Deficiency of CCAAT/enhancer-binding protein homologous protein (CHOP) prevents diet-induced aortic valve calcification in vivo.
    Aging Cell 2017 Dec 10;16(6):1334-1341. Epub 2017 Sep 10.
    Department of Cardiology, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
    Aortic valve (AoV) calcification is common in aged populations. Its subsequent aortic stenosis has been linked with increased morbidity, but still has no effective pharmacological intervention. Our previous data show endoplasmic reticulum (ER) stress is involved in AoV calcification. Read More

    Estrogenic regulation of skeletal muscle proteome: a study of premenopausal women and postmenopausal MZ cotwins discordant for hormonal therapy.
    Aging Cell 2017 Dec 7;16(6):1276-1287. Epub 2017 Sep 7.
    Medicum, Biochemistry/Developmental Biology, Meilahti Clinical Proteomics Core Facility, University of Helsinki, Helsinki, Finland.
    Female middle age is characterized by a decline in skeletal muscle mass and performance, predisposing women to sarcopenia, functional limitations, and metabolic dysfunction as they age. Menopausal loss of ovarian function leading to low circulating level of 17β-estradiol has been suggested as a contributing factor to aging-related muscle deterioration. However, the underlying molecular mechanisms remain largely unknown and thus far androgens have been considered as a major anabolic hormone for skeletal muscle. Read More

    The acceleration of reproductive aging in Nrg1(flox/flox) ;Cyp19-Cre female mice.
    Aging Cell 2017 Dec 31;16(6):1288-1299. Epub 2017 Aug 31.
    Graduate School of Biosphere Science, Hiroshima University, Higashi-Hiroshima, Japan.
    Irregular menstrual cycles, reduced responses to exogenous hormonal treatments, and altered endocrine profiles (high FSH/high LH/low AMH) are observed in women with increasing age before menopause. In this study, because the granulosa cell-specific Nrg1 knockout mice (gcNrg1KO) presented ovarian and endocrine phenotypes similar to older women, we sought to understand the mechanisms of ovarian aging and to develop a new strategy for improving fertility in older women prior to menopause. In the ovary of 6-month-old gcNrg1KO mice, follicular development was blocked in bilayer secondary follicles and heterogeneous cells accumulated in ovarian stroma. Read More

    Hyperphosphatemia induces senescence in human endothelial cells by increasing endothelin-1 production.
    Aging Cell 2017 Dec 31;16(6):1300-1312. Epub 2017 Aug 31.
    Instituto Reina Sofía de Investigación Nefrológica, IRSIN, Madrid, Spain.
    Hyperphosphatemia is related to some pathologies, affecting vascular cell behavior. This work analyzes whether high concentration of extracellular phosphate induces endothelial senescence through up-regulation of endothelin-1 (ET-1), exploring the mechanisms involved. The phosphate donor β-glycerophosphate (BGP) in human endothelial cells increased ET-1 production, endothelin-converting enzyme-1 (ECE-1) protein, and mRNA expression, which depend on the AP-1 activation through ROS production. Read More

    Can FSH influence longevity?
    Aging Cell 2017 Oct 30;16(5):916-917. Epub 2017 Aug 30.
    Department of Internal Medicine, SIU School of Medicine, 801 N. Rutledge, P.O. Box 19628, Springfield, IL, 62704-9628, USA.
    It was recently reported that the extragonadal actions of follicle-stimulating hormone (FSH) include regulation of brown and white adipose tissue function and thermogenesis. Based on these findings and on our evidence for reduced FSH levels and enhanced thermogenesis in long-lived growth hormone (GH)-deficient mice and GH-resistant mice, we suggest that FSH may have a role in the control of aging and longevity. We speculate that alterations in FSH secretion may represent one of the mechanisms of trade-offs between reproduction and aging. Read More

    Wide-scale comparative analysis of longevity genes and interventions.
    Aging Cell 2017 Dec 24;16(6):1267-1275. Epub 2017 Aug 24.
    The Shraga Segal Department of Microbiology, Immunology and Genetics, Center for Multidisciplinary Research on Aging, Ben-Gurion University of the Negev, POB 653, Beer Sheva, 8410501, Israel.
    Hundreds of genes, when manipulated, affect the lifespan of model organisms (yeast, worm, fruit fly, and mouse) and thus can be defined as longevity-associated genes (LAGs). A major challenge is to determine whether these LAGs are model-specific or may play a universal role as longevity regulators across diverse taxa. A wide-scale comparative analysis of the 1805 known LAGs across 205 species revealed that (i) LAG orthologs are substantially overrepresented, from bacteria to mammals, compared to the entire genomes or interactomes, and this was especially noted for essential LAGs; (ii) the effects on lifespan, when manipulating orthologous LAGs in different model organisms, were mostly concordant, despite a high evolutionary distance between them; (iii) LAGs that have orthologs across a high number of phyla were enriched in translational processes, energy metabolism, and DNA repair genes; (iv) LAGs that have no orthologs out of the taxa in which they were discovered were enriched in autophagy (Ascomycota/Fungi), G proteins (Nematodes), and neuroactive ligand-receptor interactions (Chordata). Read More

    Sex differences in lifespan extension with acarbose and 17-α estradiol: gonadal hormones underlie male-specific improvements in glucose tolerance and mTORC2 signaling.
    Aging Cell 2017 Dec 22;16(6):1256-1266. Epub 2017 Aug 22.
    Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
    Interventions that extend lifespan in mice can show substantial sexual dimorphism. Here, we show that male-specific lifespan extension with two pharmacological treatments, acarbose (ACA) and 17-α estradiol (17aE2), is associated, in males only, with increased insulin sensitivity and improved glucose tolerance. Females, which show either smaller (ACA) or no lifespan extension (17aE2), do not derive these metabolic benefits from drug treatment. Read More

    In aged primary T cells, mitochondrial stress contributes to telomere attrition measured by a novel imaging flow cytometry assay.
    Aging Cell 2017 Dec 19;16(6):1234-1243. Epub 2017 Aug 19.
    Translational Immunology Laboratory, NIHR BRC, John Radcliffe Hospital, Oxford, OX3 9DU, UK.
    The decline of the immune system with age known as immune senescence contributes to inefficient pathogen clearance and is a key risk factor for many aged-related diseases. However, reversing or halting immune aging requires more knowledge about the cell biology of senescence in immune cells. Telomere shortening, low autophagy and mitochondrial dysfunction have been shown to underpin cell senescence. Read More

    A multimethod computational simulation approach for investigating mitochondrial dynamics and dysfunction in degenerative aging.
    Aging Cell 2017 Dec 16;16(6):1244-1255. Epub 2017 Aug 16.
    Center for Environmental Medicine, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, 80523, USA.
    Research in biogerontology has largely focused on the complex relationship between mitochondrial dysfunction and biological aging. In particular, the mitochondrial free radical theory of aging (MFRTA) has been well accepted. However, this theory has been challenged by recent studies showing minimal increases in reactive oxygen species (ROS) as not entirely deleterious in nature, and even beneficial under the appropriate cellular circumstances. Read More

    Opposing effects on cardiac function by calorie restriction in different-aged mice.
    Aging Cell 2017 Oct 11;16(5):1155-1167. Epub 2017 Aug 11.
    Department of Geratology, The First Hospital Affiliated to Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, China.
    Calorie restriction (CR) increases average and maximum lifespan and exhibits an apparent beneficial impact on age-related diseases. Several studies have shown that CR initiated either in middle or old age could improve ischemic tolerance and rejuvenate the aging heart; however, the data are not uniform when initiated in young. The accurate time to initiate CR providing maximum benefits for cardiac remodeling and function during aging remains unclear. Read More

    The valosin-containing protein is a novel repressor of cardiomyocyte hypertrophy induced by pressure overload.
    Aging Cell 2017 Oct 11;16(5):1168-1179. Epub 2017 Aug 11.
    Division of Physiology, Department of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA, USA.
    Hypertension-induced left ventricular hypertrophy (LVH) is an independent risk factor for heart failure. Regression of LVH has emerged as a major goal in the treatment of hypertensive patients. Here, we tested our hypothesis that the valosin-containing protein (VCP), an ATPase associate protein, is a novel repressor of cardiomyocyte hypertrophy under the pressure overload stress. Read More

    Reduced expression of PMCA1 is associated with increased blood pressure with age which is preceded by remodelling of resistance arteries.
    Aging Cell 2017 Oct 9;16(5):1104-1113. Epub 2017 Aug 9.
    Division of Cardiovascular Sciences, Manchester Academic Health Science Centre, The University of Manchester, AV Hill Building, Manchester, M13 9PT, UK.
    Hypertension is a well-established risk factor for adverse cardiovascular events, and older age is a risk factor for the development of hypertension. Genomewide association studies have linked ATP2B1, the gene for the plasma membrane calcium ATPase 1 (PMCA1), to blood pressure (BP) and hypertension. Here, we present the effects of reduction in the expression of PMCA1 on BP and small artery structure and function when combined with advancing age. Read More

    Autophagy in stem cell aging.
    Aging Cell 2017 Oct 7;16(5):912-915. Epub 2017 Aug 7.
    Cellular Oncology Group, Biodonostia Institute, San Sebastian, Spain.
    Aging is responsible for changes in mammalian tissues that result in an imbalance to tissue homeostasis and a decline in the regeneration capacity of organs due to stem cell exhaustion. Autophagy is a constitutive pathway necessary to degrade damaged organelles and protein aggregates. Autophagy is one of the hallmarks of aging, which involves a decline in the number and functionality of stem cells. Read More

    In vivo imaging reveals mitophagy independence in the maintenance of axonal mitochondria during normal aging.
    Aging Cell 2017 Oct 7;16(5):1180-1190. Epub 2017 Aug 7.
    Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China.
    Mitophagy is thought to be a critical mitochondrial quality control mechanism in neurons and has been extensively studied in neurological disorders such as Parkinson's disease. However, little is known about how mitochondria are maintained in the lengthy neuronal axons in the context of physiological aging. Here, we utilized the unique Drosophila wing nerve model and in vivo imaging to rigorously profile changes in axonal mitochondria during aging. Read More

    Dyrk1 inhibition improves Alzheimer's disease-like pathology.
    Aging Cell 2017 Oct 4;16(5):1146-1154. Epub 2017 Aug 4.
    The Arizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, AZ, 85287, USA.
    There is an urgent need for the development of new therapeutic strategies for Alzheimer's disease (AD). The dual-specificity tyrosine phosphorylation-regulated kinase-1A (Dyrk1a) is a protein kinase that phosphorylates the amyloid precursor protein (APP) and tau and thus represents a link between two key proteins involved in AD pathogenesis. Furthermore, Dyrk1a is upregulated in postmortem human brains, and high levels of Dyrk1a are associated with mental retardation. Read More

    The ω-3 fatty acid α-linolenic acid extends Caenorhabditis elegans lifespan via NHR-49/PPARα and oxidation to oxylipins.
    Aging Cell 2017 Oct 3;16(5):1125-1135. Epub 2017 Aug 3.
    Center for Healthy Aging, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA.
    The dietary intake of ω-3 polyunsaturated fatty acids has been linked to a reduction in the incidence of aging-associated disease including cardiovascular disease and stroke. Additionally, long-lived Caenorhabditis elegans glp-1 germ line-less mutant animals show a number of changes in lipid metabolism including the increased production of the ω-3 fatty acid, α-linolenic acid (ALA). Here, we show that the treatment of C. Read More

    HDAC3 negatively regulates spatial memory in a mouse model of Alzheimer's disease.
    Aging Cell 2017 Oct 3;16(5):1073-1082. Epub 2017 Aug 3.
    The State Key Laboratory of Pharmaceutical Biotechnology, Department of Neurology, Medical School, Drum Tower Hospital, Nanjing University, Nanjing, China.
    The accumulation and deposition of beta-amyloid (Aβ) is a key neuropathological hallmark of Alzheimer's disease (AD). Histone deacetylases (HDACs) are promising therapeutic targets for the treatment of AD, while the specific HDAC isoforms associated with cognitive improvement are poorly understood. In this study, we investigate the role of HDAC3 in the pathogenesis of AD. Read More

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