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Aging Cell

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https://www.readbyqxmd.com/read/28317242/chemical-screening-identifies-rock-as-a-target-for-recovering-mitochondrial-function-in-hutchinson-gilford-progeria-syndrome
#1
Hyun Tae Kang, Joon Tae Park, Kobong Choi, Hyo Jei Claudia Choi, Chul Won Jung, Gyu Ree Kim, Young-Sam Lee, Sang Chul Park
Hutchinson-Gilford progeria syndrome (HGPS) constitutes a genetic disease wherein an aging phenotype manifests in childhood. Recent studies indicate that reactive oxygen species (ROS) play important roles in HGPS phenotype progression. Thus, pharmacological reduction in ROS levels has been proposed as a potentially effective treatment for patient with this disorder. In this study, we performed high-throughput screening to find compounds that could reduce ROS levels in HGPS fibroblasts and identified rho-associated protein kinase (ROCK) inhibitor (Y-27632) as an effective agent...
March 19, 2017: Aging Cell
https://www.readbyqxmd.com/read/28317237/disruption-of-the-cx43-mir21-pathway-leads-to-osteocyte-apoptosis-and-increased-osteoclastogenesis-with-aging
#2
Hannah M Davis, Rafael Pacheco-Costa, Emily G Atkinson, Lucas R Brun, Arancha R Gortazar, Julia Harris, Masahiro Hiasa, Surajudeen A Bolarinwa, Toshiyuki Yoneda, Mircea Ivan, Angela Bruzzaniti, Teresita Bellido, Lilian I Plotkin
Skeletal aging results in apoptosis of osteocytes, cells embedded in bone that control the generation/function of bone forming and resorbing cells. Aging also decreases connexin43 (Cx43) expression in bone; and osteocytic Cx43 deletion partially mimics the skeletal phenotype of old mice. Particularly, aging and Cx43 deletion increase osteocyte apoptosis, and osteoclast number and bone resorption on endocortical bone surfaces. We examined herein the molecular signaling events responsible for osteocyte apoptosis and osteoclast recruitment triggered by aging and Cx43 deficiency...
March 19, 2017: Aging Cell
https://www.readbyqxmd.com/read/28299908/the-drugage-database-of-aging-related-drugs
#3
Diogo Barardo, Daniel Thornton, Harikrishnan Thoppil, Michael Walsh, Samim Sharifi, Susana Ferreira, Andreja Anžič, Maria Fernandes, Patrick Monteiro, Tjaša Grum, Rui Cordeiro, Evandro Araújo De-Souza, Arie Budovsky, Natali Araujo, Jan Gruber, Michael Petrascheck, Vadim E Fraifeld, Alexander Zhavoronkov, Alexey Moskalev, João Pedro de Magalhães
Aging is a major worldwide medical challenge. Not surprisingly, identifying drugs and compounds that extend lifespan in model organisms is a growing research area. Here, we present DrugAge (http://genomics.senescence.info/drugs/), a curated database of lifespan-extending drugs and compounds. At the time of writing, DrugAge contains 1316 entries featuring 418 different compounds from studies across 27 model organisms, including worms, flies, yeast and mice. Data were manually curated from 324 publications. Using drug-gene interaction data, we also performed a functional enrichment analysis of targets of lifespan-extending drugs...
March 16, 2017: Aging Cell
https://www.readbyqxmd.com/read/28295976/insulin-like-growth-factor-1-deficiency-exacerbates-hypertension-induced-cerebral-microhemorrhages-in-mice-mimicking-the-aging-phenotype
#4
Stefano Tarantini, Noa M Valcarcel-Ares, Andriy Yabluchanskiy, Zsolt Springo, Gabor A Fulop, Nicole Ashpole, Tripti Gautam, Cory B Giles, Jonathan D Wren, William E Sonntag, Anna Csiszar, Zoltan Ungvari
Clinical and experimental studies show that aging exacerbates hypertension-induced cerebral microhemorrhages (CMHs), which progressively impair neuronal function. There is growing evidence that aging promotes insulin-like growth factor 1 (IGF-1) deficiency, which compromises multiple aspects of cerebromicrovascular and brain health. To determine the role of IGF-1 deficiency in the pathogenesis of CMHs, we induced hypertension in mice with liver-specific knockdown of IGF-1 (Igf1(f/f)  + TBG-Cre-AAV8) and control mice by angiotensin II plus l-NAME treatment...
March 14, 2017: Aging Cell
https://www.readbyqxmd.com/read/28295945/parallel-evolution-of-genes-controlling-mitonuclear-balance-in-short-lived-annual-fishes
#5
Arne Sahm, Martin Bens, Matthias Platzer, Alessandro Cellerino
The current molecular understanding of the aging process derives almost exclusively from the study of random or targeted single-gene mutations in highly inbred laboratory species, mostly invertebrates. Little information is available as to the genetic mechanisms responsible for natural lifespan variation and the evolution of lifespan, especially in vertebrates. Here, we investigated the pattern of positive selection in annual (i.e., short-lived) and nonannual (i.e., longer-lived) African killifishes to identify a genomic substrate for evolution of annual life history (and reduced lifespan)...
March 11, 2017: Aging Cell
https://www.readbyqxmd.com/read/28266167/pathophysiology-of-heart-failure-and-frailty-a-common-inflammatory-origin
#6
REVIEW
Lavanya Bellumkonda, Daniel Tyrrell, Scott L Hummel, Daniel R Goldstein
Frailty, a clinical syndrome that typically occurs in older adults, implies a reduced ability to tolerate biological stressors. Frailty accompanies many age-related diseases but can also occur without overt evidence of end-organ disease. The condition is associated with circulating inflammatory cytokines and sarcopenia, features that are shared with heart failure (HF). However, the biological underpinnings of frailty remain unclear and the interaction with HF is complex. Here, we describe the inflammatory pathophysiology that is associated with frailty and speculate that the inflammation that occurs with frailty shares common origins with HF...
March 7, 2017: Aging Cell
https://www.readbyqxmd.com/read/28256090/sterol-regulatory-element-binding-protein-1c-orchestrates-metabolic-remodeling-of-white-adipose-tissue-by-caloric-restriction
#7
Namiki Fujii, Takumi Narita, Naoyuki Okita, Masaki Kobayashi, Yurika Furuta, Yoshikazu Chujo, Masahiro Sakai, Atsushi Yamada, Kanae Takeda, Tomokazu Konishi, Yuka Sudo, Isao Shimokawa, Yoshikazu Higami
Caloric restriction (CR) can delay onset of several age-related pathophysiologies and extend lifespan in various species, including rodents. CR also induces metabolic remodeling involved in activation of lipid metabolism, enhancement of mitochondrial biogenesis, and reduction of oxidative stress in white adipose tissue (WAT). In studies using genetically modified mice with extended lifespans, WAT characteristics influenced mammalian lifespans. However, molecular mechanisms underlying CR-associated metabolic remodeling of WAT remain unclear...
March 3, 2017: Aging Cell
https://www.readbyqxmd.com/read/28247585/aging-yeast-gain-a-competitive-advantage-on-non-optimal-carbon-sources
#8
Stephen Frenk, Grazia Pizza, Rachael V Walker, Jonathan Houseley
Animals, plants and fungi undergo an aging process with remarkable physiological and molecular similarities, suggesting that aging has long been a fact of life for eukaryotes and one to which our unicellular ancestors were subject. Key biochemical pathways that impact longevity evolved prior to multicellularity, and the interactions between these pathways and the aging process therefore emerged in ancient single-celled eukaryotes. Nevertheless, we do not fully understand how aging impacts the fitness of unicellular organisms, and whether such cells gain a benefit from modulating rather than simply suppressing the aging process...
March 1, 2017: Aging Cell
https://www.readbyqxmd.com/read/28229533/expansion-of-myeloid-derived-suppressor-cells-with-aging-in-the-bone-marrow-of-mice-through-a-nf-%C3%AE%C2%BAb-dependent-mechanism
#9
Rafael R Flores, Cheryl L Clauson, Joonseok Cho, Byeong-Chel Lee, Sara J McGowan, Darren J Baker, Laura J Niedernhofer, Paul D Robbins
With aging, there is progressive loss of tissue homeostasis and functional reserve, leading to an impaired response to stress and an increased risk of morbidity and mortality. A key mediator of the cellular response to damage and stress is the transcription factor NF-κB. We demonstrated previously that NF-κB transcriptional activity is upregulated in tissues from both natural aged mice and in a mouse model of a human progeroid syndrome caused by defective repair of DNA damage (ERCC1-deficient mice). We also demonstrated that genetic reduction in the level of the NF-κB subunit p65(RelA) in the Ercc1(-/∆) progeroid mouse model of accelerated aging delayed the onset of age-related pathology including muscle wasting, osteoporosis, and intervertebral disk degeneration...
February 23, 2017: Aging Cell
https://www.readbyqxmd.com/read/28185435/evidence-that-a-mitochondrial-death-spiral-underlies-antagonistic-pleiotropy
#10
REVIEW
Michael Stern
The antagonistic pleiotropy (AP) theory posits that aging occurs because alleles that are detrimental in older organisms are beneficial to growth early in life and thus are maintained in populations. Although genes of the insulin signaling pathway likely participate in AP, the insulin-regulated cellular correlates of AP have not been identified. The mitochondrial quality control process called mitochondrial autophagy (mitophagy), which is inhibited by insulin signaling, might represent a cellular correlate of AP...
February 9, 2017: Aging Cell
https://www.readbyqxmd.com/read/28185406/detecting-senescence-a-new-method-for-an-old-pigment
#11
Hanna Salmonowicz, João F Passos
Cellular senescence is a state of irreversible cell cycle arrest induced by different types of cellular stresses. The field of senescence has made significant advances in the understanding of many of the mechanisms governing this phenomenon; however, a universal biomarker that unambiguously distinguishes senescent from proliferating cells has not been found. In this issue of Aging Cell, Evangelou and colleagues developed a sensitive method for identification of senescent cells in different types of biological material based on the detection of lipofuscin using an analogue of Sudan Black B (SBB) histochemical dye coupled with biotin, which they named GL13...
February 9, 2017: Aging Cell
https://www.readbyqxmd.com/read/28181388/muscle-strength-mediates-the-relationship-between-mitochondrial-energetics-and-walking-performance
#12
Ariel C Zane, David A Reiter, Michelle Shardell, Donnie Cameron, Eleanor M Simonsick, Kenneth W Fishbein, Stephanie A Studenski, Richard G Spencer, Luigi Ferrucci
Skeletal muscle mitochondrial oxidative capacity declines with age and negatively affects walking performance, but the mechanism for this association is not fully clear. We tested the hypothesis that impaired oxidative capacity affects muscle performance and, through this mechanism, has a negative effect on walking speed. Muscle mitochondrial oxidative capacity was measured by in vivo phosphorus magnetic resonance spectroscopy as the postexercise phosphocreatine resynthesis rate, kPCr , in 326 participants (154 men), aged 24-97 years (mean 71), in the Baltimore Longitudinal Study of Aging...
February 9, 2017: Aging Cell
https://www.readbyqxmd.com/read/28156058/aging-and-caloric-restriction-impact-adipose-tissue-adiponectin-and-circulating-lipids
#13
Karl N Miller, Maggie S Burhans, Josef P Clark, Porsha R Howell, Michael A Polewski, Tyler M DeMuth, Kevin W Eliceiri, Mary J Lindstrom, James M Ntambi, Rozalyn M Anderson
Adipose tissue expansion has been associated with system-wide metabolic dysfunction and increased vulnerability to diabetes, cancer, and cardiovascular disease. A reduction in adiposity is a hallmark of caloric restriction (CR), an intervention that extends longevity and delays the onset of these same age-related conditions. Despite these parallels, the role of adipose tissue in coordinating the metabolism of aging is poorly defined. Here, we show that adipose tissue metabolism and secretory profiles change with age and are responsive to CR...
February 3, 2017: Aging Cell
https://www.readbyqxmd.com/read/28139067/the-effects-of-graded-levels-of-calorie-restriction-ix-global-metabolomic-screen-reveals-modulation-of-carnitines-sphingolipids-and-bile-acids-in-the-liver-of-c57bl-6-mice
#14
Cara L Green, Sharon E Mitchell, Davina Derous, Yingchun Wang, Luonan Chen, Jing-Dong J Han, Daniel E L Promislow, David Lusseau, Alex Douglas, John R Speakman
Calorie restriction (CR) remains the most robust intervention to extend lifespan and improve health span. Using a global mass spectrometry-based metabolomic approach, we identified 193 metabolites that were significantly differentially expressed (SDE) in the livers of C57BL/6 mice, fed graded levels of CR (10, 20, 30 and 40% CR) compared to mice fed ad libitum for 12 h a day. The differential expression of metabolites also varied with the different feeding groups. Pathway analysis revealed that graded CR had an impact on carnitine synthesis and the carnitine shuttle pathway, sphingosine-1-phosphate (S1P) signalling and methionine metabolism...
January 31, 2017: Aging Cell
https://www.readbyqxmd.com/read/28256074/erratum
#15
(no author information available yet)
No abstract text is available yet for this article.
April 2017: Aging Cell
https://www.readbyqxmd.com/read/28256073/aging-impairs-dendrite-morphogenesis-of-newborn-neurons-and-is-rescued-by-7-8-dihydroxyflavone
#16
Xiaoting Wang, Jennifer Lynn Romine, Xiang Gao, Jinhui Chen
All aging individuals will develop some degree of decline in cognitive capacity as time progresses. The molecular and cellular mechanisms leading to age-related cognitive decline are still not fully understood. Through our previous research, we discovered that active neural progenitor cells selectively become more quiescent in response to aging, thus leading to the decline of neurogenesis in the aged hippocampus. Here, we further find that aging impaired dendrite development of newborn neurons. Currently, no effective approach is available to increase neurogenesis or promote dendrite development of newborn neurons in the aging brain...
April 2017: Aging Cell
https://www.readbyqxmd.com/read/28177569/the-oxidized-thiol-proteome-in-aging-and-cataractous-mouse-and-human-lens-revealed-by-icat-labeling
#17
Benlian Wang, Grant Hom, Sheng Zhou, Minfei Guo, Binbin Li, Jing Yang, Vincent M Monnier, Xingjun Fan
Age-related cataractogenesis is associated with disulfide-linked high molecular weight (HMW) crystallin aggregates. We recently found that the lens crystallin disulfidome was evolutionarily conserved in human and glutathione-depleted mouse (LEGSKO) cataracts and that it could be mimicked by oxidation in vitro (Mol. Cell Proteomics, 14, 3211-23 (2015)). To obtain a comprehensive blueprint of the oxidized key regulatory and cytoskeletal proteins underlying cataractogenesis, we have now used the same approach to determine, in the same specimens, all the disulfide-forming noncrystallin proteins identified by ICAT proteomics...
April 2017: Aging Cell
https://www.readbyqxmd.com/read/28160413/accelerated-aging-exacerbates-a-pre-existing-pathology-in-a-tau-transgenic-mouse-model
#18
Liviu-Gabriel Bodea, Harrison Tudor Evans, Ann Van der Jeugd, Lars M Ittner, Fabien Delerue, Jillian Kril, Glenda Halliday, John Hodges, Mathew C Kiernan, Jürgen Götz
Age is a critical factor in the prevalence of tauopathies, including Alzheimer's disease. To observe how an aging phenotype interacts with and affects the pathological intracellular accumulation of hyperphosphorylated tau, the tauopathy mouse model pR5 (expressing P301L mutant human tau) was back-crossed more than ten times onto a senescence-accelerated SAMP8 background to establish the new strain, SApT. Unlike SAMP8 mice, pR5 mice are characterized by a robust tau pathology particularly in the amygdala and hippocampus...
April 2017: Aging Cell
https://www.readbyqxmd.com/read/28156052/melatonin-alleviates-lipopolysaccharide-compromised-integrity-of-blood-brain-barrier-through-activating-amp-activated-protein-kinase-in-old-mice
#19
Xiaona Wang, Gai-Xiu Xue, Wen-Cao Liu, Hui Shu, Mengwei Wang, Yanyun Sun, Xiaojing Liu, Yi Eve Sun, Chun-Feng Liu, Jie Liu, Wenlan Liu, Xinchun Jin
Blood-brain barrier (BBB) dysfunction is considered to be an early event in the pathogenesis of a variety of neurological diseases in old patients, and this could occur in old people even when facing common stress. However, the mechanism remains to be defined. In this study, we tested the hypothesis that decreased melatonin levels may account for the BBB disruption in old mice challenged with lipopolysaccharide (LPS), which mimicked the common stress of sepsis. Mice (24-28 months of age) received melatonin (10 mg kg(-1)  day(-1) , intraperitoneally, i...
April 2017: Aging Cell
https://www.readbyqxmd.com/read/28127848/mir-30c-protects-diabetic-nephropathy-by-suppressing-epithelial-to-mesenchymal-transition-in-db-db-mice
#20
Yanru Zhao, Zhongwei Yin, Huaping Li, Jiahui Fan, Shenglan Yang, Chen Chen, Dao Wen Wang
Epithelial-to-mesenchymal transition (EMT) plays a significant role in tubulointerstitial fibrosis, which is a hallmark of diabetic nephropathy. Thus, identifying the mechanisms of EMT activation could be meaningful. In this study, loss of miR-30c accompanied with increased EMT was observed in renal tubules of db/db mice and cultured HK2 cells exposed to high glucose. To further explore the roles of miR-30c in EMT and tubulointerstitial fibrosis, recombinant adeno-associated viral vector was applied to manipulate the expression of miR-30c...
April 2017: Aging Cell
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