Volume 3, Issue 8

Cardiotrophin-1: a new player in energy metabolism with potential therapeutic application

Matilde Bustos, María J Moreno-Aliaga, Jesús Prieto,

https://doi.org/10.18632/aging.100359 pp 698—699

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Bustos M, Moreno-Aliaga MJ, Prieto J, . Cardiotrophin-1: a new player in energy metabolism with potential therapeutic application. . 3:698-699. https://doi.org/10.18632/aging.100359

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Why Cell Reprogramming is Functionally Linked to Aging?

Jian Zhao, Gang Pei,

https://doi.org/10.18632/aging.100364 pp 700

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Indy knockdown in mice mimics elements of dietary restriction

Gerald I. Shulman, Stephen L. Helfand,

https://doi.org/10.18632/aging.100365 pp 701

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Inducible nitric oxide synthase (iNOS) in muscle wasting syndrome, sarcopenia, and cachexia

Derek T. Hall, Jennifer F. Ma, Sergio Di Marco, Imed-Eddine Gallouzi,

https://doi.org/10.18632/aging.100358 pp 702—715

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Hall DT, Ma JF, Di Marco S, Gallouzi I, . Inducible nitric oxide synthase (iNOS) in muscle wasting syndrome, sarcopenia, and cachexia. . 3:702-715. https://doi.org/10.18632/aging.100358

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                TY  - JOUR
                AU  - Hall, Derek T. 
                AU  - Ma, Jennifer F. 
                AU  - Di Marco, Sergio 
                AU  - Gallouzi, Imed-Eddine 
                TI  - Inducible nitric oxide synthase (iNOS) in muscle wasting syndrome, sarcopenia, and cachexia
                JO  - 
                JA  - 
                VL  - 3
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100358
                DO  - 10.18632/aging.100358
                SP  - 702
                EP  - 715
                PY  - 
                AB  - Muscle atrophy—also known as muscle wasting—is a debilitating syndrome that slowly develops with age (sarcopenia) or rapidly appears at the late stages of deadly diseases such as cancer, AIDS, and sepsis (cachexia). Despite the prevalence and the drastic detrimental effects of these two syndromes, there are currently no widely used, effective treatment options for those suffering from muscle wasting. In an attempt to identify potential therapeutic targets, the molecular mechanisms of sarcopenia and cachexia have begun to be elucidated. Growing evidence suggests that inflammatory cytokines may play an important role in the pathology of both syndromes. As one of the key cytokines involved in both sarcopenic and cachectic muscle wasting, tumor necrosis factor α (TNFα) and its downstream effectors provide an enticing target for pharmacological intervention. However, to date, no drugs targeting the TNFα signaling pathway have been successful as a remedial option for the treatment of muscle wasting. Thus, there is a need to identify new effectors in this important pathway that might prove to be more efficacious targets. Inducible nitric oxide synthase (iNOS) has recently been shown to be an important mediator of TNFα-induced cachectic muscle loss, and studies suggest that it may also play a role in sarcopenia. In addition, investigations into the mechanism of iNOS-mediated muscle loss have begun to reveal potential therapeutic strategies. In this review, we will highlight the potential for targeting the iNOS/NO pathway in the treatment of muscle loss and discuss its functional relevance in sarcopenia and cachexia.
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Polyamines in aging and disease

Nadège Minois, Didac Carmona-Gutierrez, Frank Madeo,

https://doi.org/10.18632/aging.100361 pp 716—732

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Minois N, Carmona-Gutierrez D, Madeo F, . Polyamines in aging and disease. . 3:716-732. https://doi.org/10.18632/aging.100361

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                TY  - JOUR
                AU  - Minois, Nadège 
                AU  - Carmona-Gutierrez, Didac 
                AU  - Madeo, Frank 
                TI  - Polyamines in aging and disease
                JO  - 
                JA  - 
                VL  - 3
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100361
                DO  - 10.18632/aging.100361
                SP  - 716
                EP  - 732
                PY  - 
                AB  - Polyamines are polycations that interact with negatively charged molecules such as DNA, RNA and proteins. They play multiple roles in cell growth, survival and proliferation. Changes in polyamine levels have been associated with aging and diseases. Their levels decline continuously with age and polyamine (spermidine or high-polyamine diet) supplementation increases life span in model organisms. Polyamines have also been involved in stress resistance. On the other hand, polyamines are increased in cancer cells and are a target for potential chemotherapeutic agents. In this review, we bring together these various results and draw a picture of the state of our knowledge on the roles of polyamines in aging, stress and diseases.
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Longevity and stress in Caenorhabditis elegans

Katherine I. Zhou, Zachary Pincus, Frank J. Slack,

https://doi.org/10.18632/aging.100367 pp 733—753

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Zhou KI, Pincus Z, Slack FJ, . Longevity and stress in Caenorhabditis elegans. . 3:733-753. https://doi.org/10.18632/aging.100367

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                TY  - JOUR
                AU  - Zhou, Katherine I. 
                AU  - Pincus, Zachary 
                AU  - Slack, Frank J. 
                TI  - Longevity and stress in Caenorhabditis elegans
                JO  - 
                JA  - 
                VL  - 3
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100367
                DO  - 10.18632/aging.100367
                SP  - 733
                EP  - 753
                PY  - 
                AB  - It has long been understood that many of the same manipulations that increase longevity in Caenorhabditis elegans also increase resistance to various acute stressors, and vice-versa; moreover these findings hold in more complex organisms as well. Nevertheless, the mechanistic relationship between these phenotypes remains unclear, and in many cases the overlap between stress resistance and longevity is inexact. Here we review the known connections between stress resistance and longevity, discuss instances in which these connections are absent, and summarize the theoretical explanations that have been posited for these phenomena.
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Mitochondrial electron transport chain functions in long-lived Ames dwarf mice

Kashyap B. Choksi, Jonathan E. Nuss, James H. DeFord, John Papaconstantinou,

https://doi.org/10.18632/aging.100357 pp 754—767

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Choksi KB, Nuss JE, DeFord JH, Papaconstantinou J, . Mitochondrial electron transport chain functions in long-lived Ames dwarf mice. . 3:754-767. https://doi.org/10.18632/aging.100357

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                TY  - JOUR
                AU  - Choksi, Kashyap B. 
                AU  - Nuss, Jonathan E. 
                AU  - DeFord, James H. 
                AU  - Papaconstantinou, John 
                TI  - Mitochondrial electron transport chain functions in long-lived Ames dwarf mice
                JO  - 
                JA  - 
                VL  - 3
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100357
                DO  - 10.18632/aging.100357
                SP  - 754
                EP  - 767
                PY  - 
                AB  - The age-associated decline in tissue function has been attributed to ROS-mediated oxidative damage due to mitochondrial dysfunction. The long-lived Ames dwarf mouse exhibits resistance to oxidative stress, a physiological characteristic of longevity. It is not known, however, whether there are differences in the electron transport chain (ETC) functions in Ames tissues that are associated with their longevity. In these studies we analyzed enzyme activities of ETC complexes, CI-CV and the coupled CI-CII and CII-CIII activities of mitochondria from several tissues of young, middle aged and old Ames dwarf mice and their corresponding wild type controls to identify potential mitochondrial prolongevity functions. Our studies indicate that post-mitotic heart and skeletal muscle from Ames and wild-type mice show similar changes in ETC complex activities with aging, with the exception of complex IV. Furthermore, the kidney, a slowly proliferating tissue, shows dramatic differences in ETC functions unique to the Ames mice. Our data show that there are tissue specific mitochondrial functions that are characteristic of certain tissues of the long-lived Ames mouse. We propose that this may be a factor in the determination of extended lifespan of dwarf mice.
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PaCATB, a secreted catalase protecting Podospora anserina against exogenous oxidative stress

Sandra Zintel, Dominik Bernhardt, Adelina Rogowska-Wrzesinska, Heinz D. Osiewacz,

https://doi.org/10.18632/aging.100360 pp 768—781

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Zintel S, Bernhardt D, Rogowska-Wrzesinska A, Osiewacz HD, . PaCATB, a secreted catalase protecting Podospora anserina against exogenous oxidative stress. . 3:768-781. https://doi.org/10.18632/aging.100360

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                TY  - JOUR
                AU  - Zintel, Sandra 
                AU  - Bernhardt, Dominik 
                AU  - Rogowska-Wrzesinska, Adelina 
                AU  - Osiewacz, Heinz D. 
                TI  - PaCATB, a secreted catalase protecting <i>Podospora anserina</i> against exogenous oxidative stress
                JO  - 
                JA  - 
                VL  - 3
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100360
                DO  - 10.18632/aging.100360
                SP  - 768
                EP  - 781
                PY  - 
                AB  - A differential mass spectrometry analysis of secreted proteins from juvenile and senescent Podospora anserina cultures revealed age-related differences in protein profiles. Among other proteins with decreased abundance in the secretome of senescent cultures a catalase, termed PaCATB, was identified. Genetic modulation of the abundance of PaCATB identified differential effects on the phenotype of the corresponding strains. Deletion of PaCatB resulted in decreased resistance, over-expression in increased resistance against hydrogen peroxide. While the lifespan of the genetically modified strains was found to be unaffected under standard growth conditions, increased exogenous hydrogen peroxide stress in the growth medium markedly reduced the lifespan of the PaCatB deletion strain but extended the lifespan of PaCatB over-expressors. Overall our data identify a component of the secretome of P. anserina as a new effective factor to cope with environmental stress, stress that under natural conditions is constantly applied on organisms and influences aging processes.
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Mechanisms of chemotherapy-induced human ovarian aging: double strand DNA breaks and microvascular compromise

Reza Soleimani, Elke Heytens, Zbigniew Darzynkiewicz, Kutluk Oktay,

https://doi.org/10.18632/aging.100363 pp 782—793

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Soleimani R, Heytens E, Darzynkiewicz Z, Oktay K, . Mechanisms of chemotherapy-induced human ovarian aging: double strand DNA breaks and microvascular compromise. . 3:782-793. https://doi.org/10.18632/aging.100363

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                TY  - JOUR
                AU  - Soleimani, Reza 
                AU  - Heytens, Elke 
                AU  - Darzynkiewicz, Zbigniew 
                AU  - Oktay, Kutluk 
                TI  - Mechanisms of chemotherapy-induced human ovarian aging: double strand DNA breaks and microvascular compromise
                JO  - 
                JA  - 
                VL  - 3
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100363
                DO  - 10.18632/aging.100363
                SP  - 782
                EP  - 793
                PY  - 
                AB  - The mechanism of chemotherapy-induced acceleration of ovarian aging is not fully understood. We used doxorubicin, a widely used cancer chemotherapeutic, in a variety of in vivo xenograft, and in vitro models to investigate the impact of chemotherapy-induced aging on the human ovary. Doxorubicin caused massive double-strand-DNA-breaks in primordial follicles, oocytes, and granulosa cells in a dose dependent fashion as revealed by accumulating γH2AX foci. This damage was associated with apoptotic oocyte death and resulted in the activation of ATM. It appeared that the repair response enabled a minor proportion of oocytes (34.7%) and granulosa cells (12.1%) to survive while the majority succumbed to apoptotic death. Paradoxically, inhibition of ATM by KU-55933 resulted in improved survival, probably via prevention of downstream activation of TAp63α. Furthermore, doxorubicin caused vascular and stromal damage in the human ovary, which might impair ovarian function both pre- and post-menopausally. Chemotherapy-induced premature ovarian aging appears to result from a complex process involving both the germ- and non-germ cell components of the ovary. These effects may have clinical implications in aging both for premenopausal and postmenopausal cancer survivors.
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Altered behavioral and metabolic circadian rhythms in mice with disrupted NAD⁺ oscillation

Saurabh Sahar, Veronica Nin, Maria Thereza Barbosa, Eduardo Nunes Chini, Paolo Sassone-Corsi,

https://doi.org/10.18632/aging.100368 pp 794—802

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Sahar S, Nin V, Barbosa MT, Chini EN, Sassone-Corsi P, . Altered behavioral and metabolic circadian rhythms in mice with disrupted NAD⁺ oscillation. . 3:794-802. https://doi.org/10.18632/aging.100368

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                TY  - JOUR
                AU  - Sahar, Saurabh 
                AU  - Nin, Veronica 
                AU  - Barbosa, Maria Thereza 
                AU  - Chini, Eduardo Nunes 
                AU  - Sassone-Corsi, Paolo 
                TI  - Altered behavioral and metabolic circadian rhythms in mice with disrupted NAD<sup>+</sup> oscillation
                JO  - 
                JA  - 
                VL  - 3
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100368
                DO  - 10.18632/aging.100368
                SP  - 794
                EP  - 802
                PY  - 
                AB  - The Intracellular levels of nicotinamide adenine dinucleotide (NAD+) are rhythmic and controlled by the circadian clock. However, whether NAD+ oscillation in turn contributes to circadian physiology is not fully understood. To address this question we analyzed mice mutated for the NAD+ hydrolase CD38. We found that rhythmicity of NAD+ was altered in the CD38-deficient mice. The high, chronic levels of NAD+ results in several anomalies in circadian behavior and metabolism. CD38-null mice display a shortened period length of locomotor activity and alteration in the rest-activity rhythm. Several clock genes and, interestingly, genes involved in amino acid metabolism were deregulated in CD38-null livers. Metabolomic analysis identified alterations in the circadian levels of several amino acids, specifically tryptophan levels were reduced in the CD38-null mice at a circadian time paralleling with elevated NAD+ levels. Thus, CD38 contributes to behavioral and metabolic circadian rhythms and altered NAD+ levels influence the circadian clock.
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Phosphorylation of amyloid beta (Aβ) peptides – A trigger for formation of toxic aggregates in Alzheimer's disease

Sathish Kumar, Jochen Walter,

https://doi.org/10.18632/aging.100362 pp 803—812

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Kumar S, Walter J, . Phosphorylation of amyloid beta (Aβ) peptides – A trigger for formation of toxic aggregates in Alzheimer's disease. . 3:803-812. https://doi.org/10.18632/aging.100362

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                TY  - JOUR
                AU  - Kumar, Sathish 
                AU  - Walter, Jochen 
                TI  - Phosphorylation of amyloid beta (Aβ) peptides – A trigger for formation of toxic aggregates in Alzheimer's disease
                JO  - 
                JA  - 
                VL  - 3
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100362
                DO  - 10.18632/aging.100362
                SP  - 803
                EP  - 812
                PY  - 
                AB  - Alzheimer's disease (AD) is the most common form of dementia and associated with the progressive accumulation of amyloid β-peptides (Aβ) in form of extracellular amyloid plaques in the human brain. A critical role of Aβ in the pathogenesis of AD is strongly supported by gene mutations that cause early-onset familial forms of the disease. Such mutations have been identified in the APP gene itself and in presenilin 1 and 2. Importantly, all the identified mutations commonly lead to early deposition of extracellular plaques likely by increasing the generation and/or aggregation of Aβ. However, such mutations are very rare and molecular mechanisms that might trigger aggregation and deposition of Aβ, in the most common late onset AD are largely unknown. We recently demonstrated that extracellular Aβ undergoes phosphorylation by a cell surface-localized or secreted form of protein kinase A. The phosphorylation of serine residue 8 promotes aggregation by stabilization of β-sheet conformation of Aβ and increased formation of oligomeric Aβ aggregates that represent nuclei for fibrillization. Phosphorylated Aβ was detected in the brains of transgenic mice and human AD brains and showed increased toxicity in Drosophila models as compared with non-phosphorylated Aβ. Together, these findings demonstrate a novel molecular mechanism that triggers aggregation and toxicity of Aβ. Thus, phosphorylation of Aβ could be relevant in the pathogenesis of late onset AD. The identification of extracellular protein kinase A should also stimulate pharmacological approaches to decrease Aβ phosphorylation in the therapy and/or prevention of AD.
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Aging and Circadian Disruption: Causes and Effects

Steven A. Brown, Karen Schmitt, Anne Eckert,

https://doi.org/10.18632/aging.100366 pp 813—817

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Brown SA, Schmitt K, Eckert A, . Aging and Circadian Disruption: Causes and Effects. . 3:813-817. https://doi.org/10.18632/aging.100366

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                TY  - JOUR
                AU  - Brown, Steven A. 
                AU  - Schmitt, Karen 
                AU  - Eckert, Anne 
                TI  - Aging and Circadian Disruption: Causes and Effects
                JO  - 
                JA  - 
                VL  - 3
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100366
                DO  - 10.18632/aging.100366
                SP  - 813
                EP  - 817
                PY  - 
                AB  - The relationship between aging and daily “circadian” behavior in humans is bidirectional: on the one hand, dysfunction of circadian clocks promotes age-related maladies; on the other, aging per se leads to changes and disruption in circadian behavior and physiology. For the latter case, recent research suggests that changes to both homeostatic and circadian sleep regulatory mechanisms may play a role. Could hormonal changes be in part responsible?
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Volume 3, Issue 8

Editorial Comment

Cardiotrophin-1: a new player in energy metabolism with potential therapeutic application

Matilde Bustos, María J Moreno-Aliaga, Jesús Prieto,

Editorials

Why Cell Reprogramming is Functionally Linked to Aging?

Jian Zhao, Gang Pei,

Indy knockdown in mice mimics elements of dietary restriction

Gerald I. Shulman, Stephen L. Helfand,

Reviews

Inducible nitric oxide synthase (iNOS) in muscle wasting syndrome, sarcopenia, and cachexia

Derek T. Hall, Jennifer F. Ma, Sergio Di Marco, Imed-Eddine Gallouzi,

Polyamines in aging and disease

Nadège Minois, Didac Carmona-Gutierrez, Frank Madeo,

Longevity and stress in Caenorhabditis elegans

Katherine I. Zhou, Zachary Pincus, Frank J. Slack,

Research Papers

Mitochondrial electron transport chain functions in long-lived Ames dwarf mice

Kashyap B. Choksi, Jonathan E. Nuss, James H. DeFord, John Papaconstantinou,

PaCATB, a secreted catalase protecting Podospora anserina against exogenous oxidative stress

Sandra Zintel, Dominik Bernhardt, Adelina Rogowska-Wrzesinska, Heinz D. Osiewacz,

Mechanisms of chemotherapy-induced human ovarian aging: double strand DNA breaks and microvascular compromise

Reza Soleimani, Elke Heytens, Zbigniew Darzynkiewicz, Kutluk Oktay,

Altered behavioral and metabolic circadian rhythms in mice with disrupted NAD⁺ oscillation

Saurabh Sahar, Veronica Nin, Maria Thereza Barbosa, Eduardo Nunes Chini, Paolo Sassone-Corsi,

Research Perspectives

Phosphorylation of amyloid beta (Aβ) peptides – A trigger for formation of toxic aggregates in Alzheimer's disease

Sathish Kumar, Jochen Walter,

Aging and Circadian Disruption: Causes and Effects

Steven A. Brown, Karen Schmitt, Anne Eckert,

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