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Aging Cell

Kurt A Escobar, Nathan H Cole, Christine M Mermier, Trisha A VanDusseldorp
Accumulation of dysfunctional and damaged cellular proteins and organelles occurs during aging, resulting in a disruption of cellular homeostasis and progressive degeneration and increases the risk of cell death. Moderating the accrual of these defunct components is likely a key in the promotion of longevity. While exercise is known to promote healthy aging and mitigate age-related pathologies, the molecular underpinnings of this phenomenon remain largely unclear. However, recent evidences suggest that exercise modulates the proteome...
November 15, 2018: Aging Cell
Heather L Thompson, Megan J Smithey, Jennifer L Uhrlaub, Ilija Jeftić, Mladen Jergović, Sarah E White, Noreen Currier, Anna M Lang, Afam Okoye, Byung Park, Louis J Picker, Charles D Surh, Janko Nikolich-Žugich
In youth, thymic involution curtails production of new naïve T cells, placing the onus of T-cell maintenance upon secondary lymphoid organs (SLO). This peripheral maintenance preserves the size of the T-cell pool for much of the lifespan, but wanes in the last third of life, leading to a dearth of naïve T cells in blood and SLO, and contributing to suboptimal immune defense. Both keratinocyte growth factor (KGF) and sex steroid ablation (SSA) have been shown to transiently increase the size and cellularity of the old thymus...
November 14, 2018: Aging Cell
Hyo Jeong Kim, Yeonsoo Joe, Yingqing Chen, Gyu Hwan Park, Uh-Hyun Kim, Hun Taeg Chung
Amyloid-β (Aβ) peptides, the major constituent of plaques, are generated by sequential proteolytic cleavage of the amyloid precursor protein (APP) via β-secretase (BACE1) and the γ-secretase complex. It has been proposed that the abnormal secretion and accumulation of Aβ are the initial causative events in the development of Alzheimer's disease (AD). Drugs modulating this pathway could be used for AD treatment. Previous studies indicated that carbon monoxide (CO), a product of heme oxygenase (HO)-1, protects against Aβ-induced toxicity and promotes neuroprotection...
November 9, 2018: Aging Cell
Garrett L Cornelison, Simon A Levy, Tyler Jenson, Bess Frost
The nucleus is a spherical dual-membrane bound organelle that encapsulates genomic DNA. In eukaryotes, messenger RNAs (mRNA) are transcribed in the nucleus and transported through nuclear pores into the cytoplasm for translation into protein. In certain cell types and pathological conditions, nuclei harbor tubular invaginations of the nuclear envelope known as the "nucleoplasmic reticulum." Nucleoplasmic reticulum expansion has recently been established as a mediator of neurodegeneration in tauopathies, including Alzheimer's disease...
November 9, 2018: Aging Cell
Mikolaj Ogrodnik, Hanna Salmonowicz, Vadim N Gladyshev
Understanding the aging process and ways to manipulate it is of major importance for biology and medicine. Among the many aging theories advanced over the years, the concept most consistent with experimental evidence posits the buildup of numerous forms of molecular damage as a foundation of the aging process. Here, we discuss that this concept integrates well with recent findings on cellular senescence, offering a novel view on the role of senescence in aging and age-related disease. Cellular senescence has a well-established role in cellular aging, but its impact on the rate of organismal aging is less defined...
October 22, 2018: Aging Cell
Benjamin Even, Sarah Fayad-Kobeissi, Jean-Marie Gagliolo, Roberto Motterlini, Jorge Boczkowski, Roberta Foresti, Maylis Dagouassat
Chronic obstructive pulmonary disease (COPD) is associated with lung fibroblast senescence, a process characterized by an irreversible proliferation arrest associated with secretion of inflammatory mediators. ROS production, known to induce senescence, is increased in COPD fibroblasts and mitochondria dysfunction participates in this process. Among the battery of cellular responses against oxidative stress damage, heme oxygenase (HO)-1 plays a critical role in defending the lung against oxidative stress and inflammation...
October 19, 2018: Aging Cell
Valter D Longo
The identification of conserved genes and pathways that regulate lifespan but also healthspan has resulted in an improved understanding of the link between nutrients, signal transduction proteins, and aging but has also provided evidence for the existence of multiple "longevity programs," which are selected based on the availability of nutrients. Periodic fasting and other dietary restrictions can promote entry into a long-lasting longevity program characterized by cellular protection and optimal function but can also activate regenerative processes that lead to rejuvenation, which are independent of the aging rate preceding the restricted period...
October 17, 2018: Aging Cell
Tze Pin Ng, Yanxia Lu, Robin Wai Mun Choo, Crystal Tze Ying Tan, Ma Shwe Z Nyunt, Qi Gao, Esther Wing Hei Mok, Anis Larbi
Sarcopenia, a core feature of the physical frailty syndrome, is characterized by multisystem physiological dysregulation. No study has explored qualitatively the hierarchical network of relationships among different dysregulated pathways involved in the pathogenesis of sarcopenia. We used 40 blood biomarkers belonging to community-dwelling prefrail and frail older persons to derive measures of multiple physiological pathways, and structural equation modeling to generate path network models of the multisystem physiological dysregulations associated with muscle mass and function (MMF)...
October 9, 2018: Aging Cell
Adrianna Z Herskovits, Tegan A Hunter, Nicholas Maxwell, Katherine Pereira, Charles A Whittaker, Gregorio Valdez, Leonard P Guarente
SIRT1 is an NAD+ -dependent deacetylase that functions in a variety of cells and tissues to mitigate age-associated diseases. However, it remains unknown if SIRT1 also acts to prevent pathological changes that accrue in motor neurons during aging and amyotrophic lateral sclerosis (ALS). In this study, we show that SIRT1 expression decreases in the spinal cord of wild-type mice during normal aging. Using mouse models either overexpressing or lacking SIRT1 in motor neurons, we found that SIRT1 slows age-related degeneration of motor neurons' presynaptic sites at neuromuscular junctions (NMJs)...
October 8, 2018: Aging Cell
Monica R P Elmore, Lindsay A Hohsfield, Enikö A Kramár, Lilach Soreq, Rafael J Lee, Stephanie T Pham, Allison R Najafi, Elizabeth E Spangenberg, Marcelo A Wood, Brian L West, Kim N Green
Microglia, the resident immune cell of the brain, can be eliminated via pharmacological inhibition of the colony-stimulating factor 1 receptor (CSF1R). Withdrawal of CSF1R inhibition then stimulates microglial repopulation, effectively replacing the microglial compartment. In the aged brain, microglia take on a "primed" phenotype and studies indicate that this coincides with age-related cognitive decline. Here, we investigated the effects of replacing the aged microglial compartment with new microglia using CSF1R inhibitor-induced microglial repopulation...
October 2, 2018: Aging Cell
Neetu Razdan, Themistoklis Vasilopoulos, Utz Herbig
Cells that had undergone telomere dysfunction-induced senescence secrete numerous cytokines and other molecules, collectively called the senescence-associated secretory phenotype (SASP). Although certain SASP factors have been demonstrated to promote cellular senescence in neighboring cells in a paracrine manner, the mechanisms leading to bystander senescence and the functional significance of these effects are currently unclear. Here, we demonstrate that TGF-β1, a component of the SASP, causes telomere dysfunction in normal somatic human fibroblasts in a Smad3/NOX4/ROS-dependent manner...
September 22, 2018: Aging Cell
Audrey Griveau, Clotilde Wiel, Benjamin Le Calvé, Dorian V Ziegler, Sophia Djebali, Marine Warnier, Nadine Martin, Jacqueline Marvel, David Vindrieux, Martin O Bergo, David Bernard
Hutchinson-Gilford progeria syndrome (HGPS) is a lethal premature aging that recapitulates many normal aging characteristics. This disorder is caused by mutation in the LMNA gene leading to the production of progerin which induces misshapen nuclei, cellular senescence, and aging. We previously showed that the phospholipase A2 receptor (PLA2R1) promotes senescence induced by replicative, oxidative, and oncogenic stress but its role during progerin-induced senescence and in progeria is currently unknown. Here, we show that knockdown of PLA2R1 prevented senescence induced by progerin expression in human fibroblasts and markedly delayed senescence of HGPS patient-derived fibroblasts...
September 14, 2018: Aging Cell
Xingjie Ma, Marine Warnier, Clotilde Raynard, Mylène Ferrand, Olivier Kirsh, Pierre-Antoine Defossez, Nadine Martin, David Bernard
Calcium signaling is emerging as a key pathway controlling cellular senescence, a stable cell proliferation arrest playing a fundamental role in pathophysiological conditions, such as embryonic development, wound healing, cancer, and aging. However, how calcium signaling is regulated is still only partially understood. The inositol 1, 4, 5-trisphosphate receptor type 2 (ITPR2), an endoplasmic reticulum calcium release channel, was recently shown to critically contribute to the implementation of senescence, but how ITPR2 expression is controlled is unclear...
September 14, 2018: Aging Cell
Raquel Maeso-Díaz, Martí Ortega-Ribera, Anabel Fernández-Iglesias, Diana Hide, Leticia Muñoz, Amelia J Hessheimer, Sergi Vila, Rubén Francés, Constantino Fondevila, Agustín Albillos, Carmen Peralta, Jaime Bosch, Frank Tacke, Victoria C Cogger, Jordi Gracia-Sancho
The socioeconomic and medical improvements of the last decades have led to a relevant increase in the median age of worldwide population. Although numerous studies described the impact of aging in different organs and the systemic vasculature, relatively little is known about liver function and hepatic microcirculatory status in the elderly. In this study, we aimed at characterizing the phenotype of the aged liver in a rat model of healthy aging, particularly focusing on the microcirculatory function and the molecular status of each hepatic cell type in the sinusoid...
September 8, 2018: Aging Cell
Mehrnaz Shamalnasab, Simon-Pierre Gravel, Julie St-Pierre, Lionel Breton, Sibylle Jäger, Hugo Aguilaniu
Plant extracts containing salicylates are probably the most ancient remedies to reduce fever and ease aches of all kind. Recently, it has been shown that salicylates activate adenosine monophosphate-activated kinase (AMPK), which is now considered as a promising target to slow down aging and prevent age-related diseases in humans. Beneficial effects of AMPK activation on lifespan have been discovered in the model organism Caenorhabditis elegans (C. elegans). Indeed, salicylic acid and acetylsalicylic acid extend lifespan in worms by activating AMPK and the forkhead transcription factor DAF-16/FOXO...
September 7, 2018: Aging Cell
Ying Wang, Steven S Welc, Michelle Wehling-Henricks, James G Tidball
Sarcopenia is age-related muscle wasting that lacks effective therapeutic interventions. We found that systemic ablation of tumor necrosis factor-α (TNF-α) prevented sarcopenia and prevented age-related change in muscle fiber phenotype. Furthermore, TNF-α ablation reduced the number of satellite cells in aging muscle and promoted muscle cell fusion in vivo and in vitro. Because CD68+ macrophages are important sources of TNF-α and the number of CD68+ macrophages increases in aging muscle, we tested whether macrophage-derived TNF-α affects myogenesis...
September 6, 2018: Aging Cell
Hangsak Huy, Hae Young Song, Mi Jeong Kim, Won Sam Kim, Dong Oh Kim, Jae-Eun Byun, Jungwoon Lee, Young-Jun Park, Tae-Don Kim, Suk Ran Yoon, Eun-Ji Choi, Chul-Ho Lee, Ji-Yoon Noh, Haiyoung Jung, Inpyo Choi
Aging is associated with an inevitable and universal loss of cell homeostasis and restricts an organism's lifespan by an increased susceptibility to diseases and tissue degeneration. The glucose uptake associated with producing energy for cell survival is one of the major causes of ROS production under physiological conditions. However, the overall mechanisms by which glucose uptake results in cellular senescence remain mysterious. In this study, we found that TXNIP deficiency accelerated the senescent phenotypes of MEF cells under high glucose condition...
August 31, 2018: Aging Cell
Robert Büttner, Alexander Schulz, Michael Reuter, Asha K Akula, Thomas Mindos, Annemarie Carlstedt, Lars B Riecken, Stephan L Baader, Reinhard Bauer, Helen Morrison
The regenerative capacity of peripheral nerves declines during aging, contributing to the development of neuropathies, limiting organism function. Changes in Schwann cells prompt failures in instructing maintenance and regeneration of aging nerves; molecular mechanisms of which have yet to be delineated. Here, we identified an altered inflammatory environment leading to a defective Schwann cell response, as an underlying mechanism of impaired nerve regeneration during aging. Chronic inflammation was detected in intact uninjured old nerves, characterized by increased macrophage infiltration and raised levels of monocyte chemoattractant protein 1 (MCP1) and CC chemokine ligand 11 (CCL11)...
August 31, 2018: Aging Cell
Nicolas Musi, Joseph M Valentine, Kathryn R Sickora, Eric Baeuerle, Cody S Thompson, Qiang Shen, Miranda E Orr
Tau protein accumulation is the most common pathology among degenerative brain diseases, including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), traumatic brain injury (TBI) and over twenty others. Tau-containing neurofibrillary tangle (NFT) accumulation is the closest correlate with cognitive decline and cell loss (Arriagada et al., 1992), yet mechanisms mediating tau toxicity are poorly understood. NFT formation does not induce apoptosis (de Calignon et al., 2009), which suggests secondary mechanisms are driving toxicity...
August 20, 2018: Aging Cell
Jéssica M Vilas, Carmen Carneiro, Sabela Da Silva-Álvarez, Alba Ferreirós, Patricia González, María Gómez, Sagrario Ortega, Manuel Serrano, Tomás García-Caballero, Miguel González-Barcia, Anxo Vidal, Manuel Collado
Aging is characterized by a gradual functional decline of tissues with age. Adult stem and progenitor cells are responsible for tissue maintenance, repair, and regeneration, but during aging, this population of cells is decreased or its activity is reduced, compromising tissue integrity and causing pathologies that increase vulnerability, and ultimately lead to death. The causes of stem cell exhaustion during aging are not clear, and whether a reduction in stem cell function is a cause or a consequence of aging remains unresolved...
October 2018: Aging Cell
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