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      Current aging research in China

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          Abstract

          The mini-review stemmed from a recent meeting on national aging research strategies in China discusses the components and challenges of aging research in China. Highlighted are the major efforts of a number of research teams, funding situations and outstanding examples of recent major research achievements. Finally, authors discuss potential targets and strategies of aging research in China.

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          The telomere syndromes.

          Mary Armanios, Elizabeth H Blackburn (2012)
          There has been mounting evidence of a causal role for telomere dysfunction in a number of degenerative disorders. Their manifestations encompass common disease states such as idiopathic pulmonary fibrosis and bone marrow failure. Although these disorders seem to be clinically diverse, collectively they comprise a single syndrome spectrum defined by the short telomere defect. Here we review the manifestations and unique genetics of telomere syndromes. We also discuss their underlying molecular mechanisms and significance for understanding common age-related disease processes.
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            Rapamycin slows aging in mice.

            John Wilkinson, Lisa Burmeister, Susan V. Brooks … (2012)
            Rapamycin increases lifespan in mice, but whether this represents merely inhibition of lethal neoplastic diseases, or an overall slowing in multiple aspects of aging is currently unclear. We report here that many forms of age-dependent change, including alterations in heart, liver, adrenal glands, endometrium, and tendon, as well as age-dependent decline in spontaneous activity, occur more slowly in rapamycin-treated mice, suggesting strongly that rapamycin retards multiple aspects of aging in mice, in addition to any beneficial effects it may have on neoplastic disease. We also note, however, that mice treated with rapamycin starting at 9 months of age have significantly higher incidence of testicular degeneration and cataracts; harmful effects of this kind will guide further studies on timing, dosage, and tissue-specific actions of rapamycin relevant to the development of clinically useful inhibitors of TOR action. © 2012 The Authors. Aging Cell © 2012 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland.
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              Genomic instability in laminopathy-based premature aging.

              Baohua Liu, Jianming Wang, Kui Ming Chan … (2005)
              Premature aging syndromes often result from mutations in nuclear proteins involved in the maintenance of genomic integrity. Lamin A is a major component of the nuclear lamina and nuclear skeleton. Truncation in lamin A causes Hutchinson-Gilford progerial syndrome (HGPS), a severe form of early-onset premature aging. Lack of functional Zmpste24, a metalloproteinase responsible for the maturation of prelamin A, also results in progeroid phenotypes in mice and humans. We found that Zmpste24-deficient mouse embryonic fibroblasts (MEFs) show increased DNA damage and chromosome aberrations and are more sensitive to DNA-damaging agents. Bone marrow cells isolated from Zmpste24-/- mice show increased aneuploidy and the mice are more sensitive to DNA-damaging agents. Recruitment of p53 binding protein 1 (53BP1) and Rad51 to sites of DNA lesion is impaired in Zmpste24-/- MEFs and in HGPS fibroblasts, resulting in delayed checkpoint response and defective DNA repair. Wild-type MEFs ectopically expressing unprocessible prelamin A show similar defects in checkpoint response and DNA repair. Our results indicate that unprocessed prelamin A and truncated lamin A act dominant negatively to perturb DNA damage response and repair, resulting in genomic instability which might contribute to laminopathy-based premature aging.
              Article 0 comments Cited 194 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Ruijuan Sun: sunrj@nsfc.gov.cn
                Erdan Dong: donged@nsfc.gov.cn
                Journal
                Journal ID (nlm-ta): Protein Cell
                Journal ID (iso-abbrev): Protein Cell
                Title: Protein & Cell
                Publisher: Higher Education Press (Beijing )
                ISSN (Print): 1674-800X
                ISSN (Electronic): 1674-8018
                Publication date (Electronic): 18 March 2015
                Publication date PMC-release: 18 March 2015
                Publication date (Print): May 2015
                Volume: 6
                Issue: 5
                Pages: 314-321
                Affiliations
                [ ]Department of Health Sciences, National Natural Science Foundation of China, Beijing, 100085 China
                [ ]Institute of Aging Research, School of Medicine, Hangzhou Normal University, Hangzhou, 311121 China
                Article
                Publisher ID: 145
                DOI: 10.1007/s13238-015-0145-5
                PMC ID: 4417678
                PubMed ID: 25779341
                SO-VID: c532eebd-ba0b-463e-a43c-a6a6f536fee7
                Copyright © © The Author(s) 2015
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

                History
                Date received : 25 December 2014
                Date accepted : 21 January 2015
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © HEP and Springer 2015

                Keywords: aging research,funding,objectives and strategies
                Data availability:
                Keywords: aging research, funding, objectives and strategies

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