Volume 3, Issue 1

SIRT3: Striking at the heart of aging

Yufei Liu, Dan Zhang, Danica Chen,

https://doi.org/10.18632/aging.100256 pp 1—2

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Liu Y, Zhang D, Chen D, . SIRT3: Striking at the heart of aging. . 3:1-2. https://doi.org/10.18632/aging.100256

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Be quiet and you'll keep young: does mTOR underlie p53 action in protecting against senescence by favoring quiescence?

Vjekoslav Dulic,

https://doi.org/10.18632/aging.100257 pp 3—4

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The role of glyoxalases for sugar stress and aging, with relevance for dyskinesia, anxiety, dementia and Parkinson's disease

Georg Auburger, Alexander Kurz,

https://doi.org/10.18632/aging.100258 pp 5—9

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Auburger G, Kurz A, . The role of glyoxalases for sugar stress and aging, with relevance for dyskinesia, anxiety, dementia and Parkinson's disease. . 3:5-9. https://doi.org/10.18632/aging.100258

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Regulation of the mitochondrial transition pore: impact on mammalian aging

Heinz D. Osiewacz,

https://doi.org/10.18632/aging.100259 pp 10—11

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Sirt3 targets mPTP and prevents aging in the heart

Junichi Sadoshima,

https://doi.org/10.18632/aging.100266 pp 12—13

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Treating transgenic Alzheimer mice with a β-secretase inhibitor, what have we learned?

Jordan Tang, Arun Ghosh,

https://doi.org/10.18632/aging.100267 pp 14—16

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The glyoxalase system as an example of a cellular maintenance pathway with relevance to aging

Axel Kowald,

https://doi.org/10.18632/aging.100268 pp 17—18

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Manipulating ovarian aging: A new frontier in fertility preservation

Kutluk Oktay, Sumanta Goswami, Zbigniew Darzynkiewicz,

https://doi.org/10.18632/aging.100269 pp 19—21

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Cellular proteome, coregulators, endocrine system and the human brain: the Regulatory biology of humanism

Bert W. O'Malley,

https://doi.org/10.18632/aging.100270 pp 22—25

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p53 governs telomere regulation feedback too, via TRF2

Izumi Horikawa, Kaori Fujita, Curtis C. Harris,

https://doi.org/10.18632/aging.100271 pp 26—32

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Horikawa I, Fujita K, Harris CC, . p53 governs telomere regulation feedback too, via TRF2. . 3:26-32. https://doi.org/10.18632/aging.100271

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Provider: 
 TY - JOUR
 AU - Horikawa, Izumi 
 AU - Fujita, Kaori 
 AU - Harris, Curtis C. 
 TI - p53 governs telomere regulation feedback too, via TRF2
 JO - 
 JA - 
 VL - 3
 IS - 1
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.100271
 DO - 10.18632/aging.100271
 SP - 26
 EP - 32
 PY - 
 AB - p53 takes critical part in a number of positive and negative feedback loops to regulate carcinogenesis, aging and other biological processes. Uncapped or dysfunctional telomeres are an endogenous DNA damage that activates ATM kinase (ataxia telangiectasia mutated) and then p53 to induce cellular senescence or apoptosis. Our recent study shows that p53, a downstream effector of the telomere damage signaling, also functions upstream of the telomere-capping protein complex by inhibiting one of its components, TRF2 (telomeric repeat binding factor 2). Since TRF2 inhibition leads to ATM activation, a novel positive feedback loop exists to amplify uncapped telomere-induced, p53-mediated cellular responses. Siah1 (seven in absentia homolog 1), a p53-inducible E3 ubiquitin ligase, plays a key role in this feedback regulation by targeting TRF2 for ubiquitination and proteasomal degradation. Biological significance and therapeutic implications of this study are discussed.
 ER -

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HIF-1α antagonizes p53-mediated apoptosis by triggering HIPK2 degradation

Lavinia Nardinocchi, Rosa Puca, Gabriella D'Orazi,

https://doi.org/10.18632/aging.100254 pp 33—43

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Nardinocchi L, Puca R, D'Orazi G, . HIF-1α antagonizes p53-mediated apoptosis by triggering HIPK2 degradation. . 3:33-43. https://doi.org/10.18632/aging.100254

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Provider: 
                TY  - JOUR
                AU  - Nardinocchi, Lavinia 
                AU  - Puca, Rosa 
                AU  - D'Orazi, Gabriella 
                TI  - HIF-1α antagonizes p53-mediated apoptosis by triggering HIPK2 degradation
                JO  - 
                JA  - 
                VL  - 3
                IS  - 1
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100254
                DO  - 10.18632/aging.100254
                SP  - 33
                EP  - 43
                PY  - 
                AB  - Many human diseases are characterized by the development of tissue hypoxia. Hypoxia-inducible factor (HIF) is a transcription factor that regulates fundamental cellular processes in response to changes in oxygen concentration, such as angiogenesis, survival, and alterations in metabolism. The levels of HIF-1α subunit are increased in most solid tumors not only by low oxygen but also by growth factors and oncogenes and correlate with patient prognosis and treatment failure. The link between HIF-1α and apoptosis, a major determinant of cancer progression and treatment outcome, is poorly understood. Here we show that HIF-1α protects against drug-induced apoptosis by antagonizing the function of the tumor suppressor p53. HIF-1α upregulation induced proteasomal degradation of homeodomain-interacting protein kinase-2 (HIPK2), the p53 apoptotic activator. Inhibition of HIF-1α by siRNA, HIF-1α-dominant negative or by zinc re-established the HIPK2 levels and the p53-mediated chemosensitivity in tumor cells. Our findings identify a novel circuitry between HIF-1α and p53, and provide a paradigm for HIPK2 dictating cell response to antitumor therapies.
                ER  -

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Alterations of retinal pigment epithelium cause AMD-like retinopathy in senescence-accelerated OXYS rats

Anton M. Markovets, Valeriya B. Saprunova, Anna A. Zhdankina, Anzhella Zh. Fursova, Lora E. Bakeeva, Natalia G. Kolosova,

https://doi.org/10.18632/aging.100243 pp 44—54

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Markovets AM, Saprunova VB, Zhdankina AA, Fursova AZ, Bakeeva LE, Kolosova NG, . Alterations of retinal pigment epithelium cause AMD-like retinopathy in senescence-accelerated OXYS rats. . 3:44-54. https://doi.org/10.18632/aging.100243

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Provider: 
                TY  - JOUR
                AU  - Markovets, Anton M. 
                AU  - Saprunova, Valeriya B. 
                AU  - Zhdankina, Anna A. 
                AU  - Fursova, Anzhella Zh. 
                AU  - Bakeeva, Lora E. 
                AU  - Kolosova, Natalia G. 
                TI  - Alterations of retinal pigment epithelium cause AMD-like retinopathy in senescence-accelerated OXYS rats
                JO  - 
                JA  - 
                VL  - 3
                IS  - 1
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100243
                DO  - 10.18632/aging.100243
                SP  - 44
                EP  - 54
                PY  - 
                AB  - Pathogenesis of age-related macular degeneration (AMD), the leading cause of blindness in the world, remains poorly understood. This makes it necessary to create animal models for studying AMD pathogenesis and to design new therapeutic approaches. Here we showed that retinopathy in OXYS rats is similar to human AMD according to clinical signs, morphology, and vascular endothelium growth factor (VEGF) and pigment epithelium-derived factor (PEDF) genes expression. Clinical signs of retinopathy OXYS rats manifest by the age 3 months against the background of significantly reduced expression level of VEGF and PEDF genes due to the decline of the amount of retinal pigment epithelium (RPE) cells and alteration of choroidal microcirculation. The disruption in OXYS rats' retina starts at the age of 20 days and appears as reduce the area of RPE cells but does not affect their ultrastructure. Ultrastructural pathological alterations of RPE as well as develop forms of retinopathy are observed in OXYS rats from age 12 months and manifested as excessive accumulation of lipofuscin in RPE regions adjacent to the rod cells, whirling extentions of the basement membrane into the cytoplasm. These data suggest that primary cellular degenerative alterations in the RPE cells secondarily lead to choriocapillaris atrophy and results in complete loss of photoreceptor cells in the OXYS rats' retina by the age of 24 months.
                ER  -

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Polymorphisms associated with type 2 diabetes in familial longevity: The Leiden Longevity Study

Simon P. Mooijaart, Diana van Heemst, Raymond Noordam, Maarten P. Rozing, Carolien A. Wijsman, Anton J.M. de Craen, Rudi G.J. Westendorp, Marian Beekman, Eline P. Slagboom,

https://doi.org/10.18632/aging.100250 pp 55—62

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Mooijaart SP, van Heemst D, Noordam R, Rozing MP, Wijsman CA, de Craen AJ, Westendorp RG, Beekman M, Slagboom EP, . Polymorphisms associated with type 2 diabetes in familial longevity: The Leiden Longevity Study. . 3:55-62. https://doi.org/10.18632/aging.100250

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                TY  - JOUR
                AU  - Mooijaart, Simon P. 
                AU  - van Heemst, Diana 
                AU  - Noordam, Raymond 
                AU  - Rozing, Maarten P. 
                AU  - Wijsman, Carolien A. 
                AU  - de Craen, Anton J.M. 
                AU  - Westendorp, Rudi G.J. 
                AU  - Beekman, Marian 
                AU  - Slagboom, Eline P. 
                TI  - Polymorphisms associated with type 2 diabetes in familial longevity: The Leiden Longevity Study
                JO  - 
                JA  - 
                VL  - 3
                IS  - 1
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100250
                DO  - 10.18632/aging.100250
                SP  - 55
                EP  - 62
                PY  - 
                AB  - Human longevity is in part genetically determined, and the insulin/IGF-1 signal transduction (IIS) pathway has consistently been implicated. In humans, type 2 diabetes is a frequent disease that results from loss of glucose homeostasis and for which new candidate polymorphisms now rapidly emerge from genome wide association studies. In the Leiden Longevity Study (n=2415), the offspring of long lived siblings (“offspring”) who are genetically enriched for longevity were shown to have a more beneficial metabolic profile compared to their environmentally matched partners (“controls”), including better glucose tolerance. We tested whether the “offspring” carry a lower burden of diabetes risk alleles. Fifteen polymorphisms derived from genome wide association (GWA) scans in type 2 diabetes were tested for association with parameters of glucose metabolism in offspring and controls, and burden of risk alleles was compared between offspring and controls. Among all participants, a higher number of type 2 diabetes risk alleles associated with a higher prevalence of diabetes (P=0.011) and higher serum concentration of glucose (P&lt;0.016) but not insulin (P=0.450). None of the polymorphisms differed in frequency between the offspring and controls (all P&gt;0.05), nor did the mean total number of risk alleles (P=0.977). The association between polymorphisms and glucose levels did not differ between controls and offspring (Pinteraction=0.523). The better glucose tolerance of the “offspring” is not explained by a lower burden of type 2 diabetes risk alleles, suggesting that specific mechanisms determining longevity exist.
                ER  -

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Health and function of participants in the Long Life Family Study: A comparison with other cohorts

Anne B. Newman, Nancy W. Glynn, Christopher A. Taylor, Paola Sebastiani, Thomas T. Perls, Richard Mayeux, Kaare Christensen, Joseph M. Zmuda, Sandra Barral, Joseph H. Lee, Eleanor M. Simonsick, Jeremy D. Walston, Anatoli I. Yashin, Evan Hadley,

https://doi.org/10.18632/aging.100242 pp 63—76

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Newman AB, Glynn NW, Taylor CA, Sebastiani P, Perls TT, Mayeux R, Christensen K, Zmuda JM, Barral S, Lee JH, Simonsick EM, Walston JD, Yashin AI, et al, . Health and function of participants in the Long Life Family Study: A comparison with other cohorts. . 3:63-76. https://doi.org/10.18632/aging.100242

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Provider: 
                TY  - JOUR
                AU  - Newman, Anne B. 
                AU  - Glynn, Nancy W. 
                AU  - Taylor, Christopher A. 
                AU  - Sebastiani, Paola 
                AU  - Perls, Thomas T. 
                AU  - Mayeux, Richard 
                AU  - Christensen, Kaare 
                AU  - Zmuda, Joseph M. 
                AU  - Barral, Sandra 
                AU  - Lee, Joseph H. 
                AU  - Simonsick, Eleanor M. 
                AU  - Walston, Jeremy D. 
                AU  - Yashin, Anatoli I. 
                AU  - Hadley, Evan 
                TI  - Health and function of participants in the Long Life Family Study: A comparison with other cohorts
                JO  - 
                JA  - 
                VL  - 3
                IS  - 1
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100242
                DO  - 10.18632/aging.100242
                SP  - 63
                EP  - 76
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Newman, Anne B. 
                AU  - Glynn, Nancy W. 
                AU  - Taylor, Christopher A. 
                AU  - Sebastiani, Paola 
                AU  - Perls, Thomas T. 
                AU  - Mayeux, Richard 
                AU  - Christensen, Kaare 
                AU  - Zmuda, Joseph M. 
                AU  - Barral, Sandra 
                AU  - Lee, Joseph H. 
                AU  - Simonsick, Eleanor M. 
                AU  - Walston, Jeremy D. 
                AU  - Yashin, Anatoli I. 
                AU  - Hadley, Evan 
                TI  - Health and function of participants in the Long Life Family Study: A comparison with other cohorts
                JO  - 
                JA  - 
                VL  - 3
                IS  - 1
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100242
                DO  - 10.18632/aging.100242
                SP  - 63
                EP  - 76
                PY  - 
                AB  - Individuals from families recruited for the Long Life Family Study (LLFS) (n= 4559) were examined and compared to individuals from other cohorts to determine whether the recruitment targeting longevity resulted in a cohort of individuals with better health and function. Other cohorts with similar data included the Cardiovascular Health Study, the Framingham Heart Study, and the New England Centenarian Study. Diabetes, chronic pulmonary disease and peripheral artery disease tended to be less common in LLFS probands and offspring compared to similar aged persons in the other cohorts. Pulse pressure and triglycerides were lower, high density lipids were higher, and a perceptual speed task and gait speed were better in LLFS. Age-specific comparisons showed differences that would be consistent with a higher peak, later onset of decline or slower rate of change across age in LLFS participants. These findings suggest several priority phenotypes for inclusion in future genetic analysis to identify loci contributing to exceptional survival.
                ER  -

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Volume 3, Issue 1

Commentaries

SIRT3: Striking at the heart of aging

Yufei Liu, Dan Zhang, Danica Chen,

Be quiet and you'll keep young: does mTOR underlie p53 action in protecting against senescence by favoring quiescence?

Vjekoslav Dulic,

The role of glyoxalases for sugar stress and aging, with relevance for dyskinesia, anxiety, dementia and Parkinson's disease

Georg Auburger, Alexander Kurz,

Regulation of the mitochondrial transition pore: impact on mammalian aging

Heinz D. Osiewacz,

Sirt3 targets mPTP and prevents aging in the heart

Junichi Sadoshima,

Treating transgenic Alzheimer mice with a β-secretase inhibitor, what have we learned?

Jordan Tang, Arun Ghosh,

The glyoxalase system as an example of a cellular maintenance pathway with relevance to aging

Axel Kowald,

Manipulating ovarian aging: A new frontier in fertility preservation

Kutluk Oktay, Sumanta Goswami, Zbigniew Darzynkiewicz,

Essay

Cellular proteome, coregulators, endocrine system and the human brain: the Regulatory biology of humanism

Bert W. O'Malley,

Research Perspective

p53 governs telomere regulation feedback too, via TRF2

Izumi Horikawa, Kaori Fujita, Curtis C. Harris,

Research Papers

HIF-1α antagonizes p53-mediated apoptosis by triggering HIPK2 degradation

Lavinia Nardinocchi, Rosa Puca, Gabriella D'Orazi,

Alterations of retinal pigment epithelium cause AMD-like retinopathy in senescence-accelerated OXYS rats

Anton M. Markovets, Valeriya B. Saprunova, Anna A. Zhdankina, Anzhella Zh. Fursova, Lora E. Bakeeva, Natalia G. Kolosova,

Polymorphisms associated with type 2 diabetes in familial longevity: The Leiden Longevity Study

Simon P. Mooijaart, Diana van Heemst, Raymond Noordam, Maarten P. Rozing, Carolien A. Wijsman, Anton J.M. de Craen, Rudi G.J. Westendorp, Marian Beekman, Eline P. Slagboom,

Clinical Research Paper

Health and function of participants in the Long Life Family Study: A comparison with other cohorts

Anne B. Newman, Nancy W. Glynn, Christopher A. Taylor, Paola Sebastiani, Thomas T. Perls, Richard Mayeux, Kaare Christensen, Joseph M. Zmuda, Sandra Barral, Joseph H. Lee, Eleanor M. Simonsick, Jeremy D. Walston, Anatoli I. Yashin, Evan Hadley,

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