1,540 results match your criteria Aging Cell [Journal]
Aging Cell 2018 Jun 19:e12792. Epub 2018 Jun 19.
Lipid Science and Aging Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan.
Dysregulation of plasma lipids is associated with age-related cardiovascular diseases. L5, the most electronegative subfraction of chromatographically resolved low-density lipoprotein (LDL), induces endothelial dysfunction, whereas the least electronegative subfraction, L1, does not. In this study, we examined the effects of L5 on endothelial senescence and its underlying mechanisms. Read More
Aging Cell 2018 Jun 14:e12798. Epub 2018 Jun 14.
Frontier Research Core for Life Sciences, University of Toyama, Toyama, Japan.
Nicotinamide adenine dinucleotide (NAD) is an important cofactor that regulates various biological processes, including metabolism and gene expression. As a coenzyme, NAD controls mitochondrial respiration through enzymes of the tricarboxylic acid (TCA) cycle, β-oxidation, and oxidative phosphorylation and also serves as a substrate for posttranslational protein modifications, such as deacetylation and ADP-ribosylation by sirtuins and poly(ADP-ribose) polymerase (PARP), respectively. Many studies have demonstrated that NAD levels decrease with aging and that these declines cause various aging-associated diseases. Read More
Aging Cell 2018 Jun 12:e12794. Epub 2018 Jun 12.
Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
The alteration of age-related molecules in the bone marrow microenvironment is one of the driving forces in osteoporosis. These molecules inhibit bone formation and promote bone resorption by regulating osteoblastic and osteoclastic activity, contributing to age-related bone loss. Here, we observed that the level of microRNA-31a-5p (miR-31a-5p) was significantly increased in bone marrow stromal cells (BMSCs) from aged rats, and these BMSCs demonstrated increased adipogenesis and aging phenotypes as well as decreased osteogenesis and stemness. Read More
Aging Cell 2018 Jun 11:e12793. Epub 2018 Jun 11.
INSERM U955, équipe 3, Créteil, France.
The cellular mechanisms responsible for aging are poorly understood. Aging is considered as a degenerative process induced by the accumulation of cellular lesions leading progressively to organ dysfunction and death. The free radical theory of aging has long been considered the most relevant to explain the mechanisms of aging. Read More
Aging Cell 2018 Jun 7:e12790. Epub 2018 Jun 7.
Department of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam Neuroscience, Amsterdam, The Netherlands.
Microglia dynamically adapt their morphology and function during increasing age. However, the mechanisms behind these changes are to date poorly understood. Glucocorticoids (GCs) are long known and utilized for their immunomodulatory actions and endogenous GC levels are described to alter with advancing age. Read More
Aging Cell 2018 Jun 6:e12791. Epub 2018 Jun 6.
Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, California.
Alzheimer's disease (AD) is a devastating neurodegenerative disorder that impairs memory and causes cognitive and psychiatric deficits. New evidences indicate that AD is conceptualized as a disease of synaptic failure, although the molecular and cellular mechanisms underlying these defects remain to be elucidated. Determining the timing and nature of the early synaptic deficits is critical for understanding the progression of the disease and for identifying effective targets for therapeutic intervention. Read More
Aging Cell 2018 Jun 5:e12787. Epub 2018 Jun 5.
Department of Psychiatry, New York University School of Medicine, New York, New York.
Mounting evidence suggests that mitochondrial dysfunction plays a causal role in the etiology and progression of Alzheimer's disease (AD). We recently showed that the carbonic anhydrase inhibitor (CAI) methazolamide (MTZ) prevents amyloid β (Aβ)-mediated onset of apoptosis in the mouse brain. In this study, we used MTZ and, for the first time, the analog CAI acetazolamide (ATZ) in neuronal and cerebral vascular cells challenged with Aβ, to clarify their protective effects and mitochondrial molecular mechanism of action. Read More
Aging Cell 2018 Jun 4:e12788. Epub 2018 Jun 4.
Key Laboratory of Agricultural Animal Genetics, Breeding, and Reproduction of the Ministry of Education & Key Laboratory of Swine Genetics and Breeding of Ministry of Agriculture, Huazhong Agricultural University, Wuhan, China.
Satellite cells play a key role in the aging, generation, and damage repair of skeletal muscle. The molecular mechanism of satellite cells in these processes remains largely unknown. This study systematically investigated for the first time the characteristics of mouse satellite cells at ten different ages. Read More
Aging Cell 2018 May 30:e12776. Epub 2018 May 30.
Division of Plastic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, MO, USA.
Neuromuscular decline occurs with aging. The neuromuscular junction (NMJ), the interface between motor nerve and muscle, also undergoes age-related changes. Aging effects on the NMJ components-motor nerve terminal, acetylcholine receptors (AChRs), and nonmyelinating terminal Schwann cells (tSCs)-have not been comprehensively evaluated. Read More
Aging Cell 2018 May 30:e12784. Epub 2018 May 30.
Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut.
Caseinolytic peptidase P mediates degradation of unfolded mitochondrial proteins and activates mitochondrial unfolded protein response (mtUPR) to maintain protein homeostasis. Clpp female mice generate a lower number of mature oocytes and two-cell embryos, and no blastocysts. Clpp oocytes have smaller mitochondria, with lower aspect ratio (length/width), and decreased expression of genes that promote fusion. Read More
Aging Cell 2018 May 29:e12789. Epub 2018 May 29.
State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.
SIRT4 modulates energy homeostasis in multiple cell types and tissues. However, its role in meiotic oocytes remains unknown. Here, we report that mouse oocytes overexpressing SIRT4 are unable to completely progress through meiosis, showing the inadequate mitochondrial redistribution, lowered ATP content, elevated reactive oxygen species (ROS) level, with the severely disrupted spindle/chromosome organization. Read More
Aging Cell 2018 May 29:e12777. Epub 2018 May 29.
Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, New York.
Inability to preserve proteostasis with age contributes to the gradual loss of function that characterizes old organisms. Defective autophagy, a component of the proteostasis network for delivery and degradation of intracellular materials in lysosomes, has been described in multiple old organisms, while a robust autophagy response has been linked to longevity. The molecular mechanisms responsible for defective autophagic function with age remain, for the most part, poorly characterized. Read More
Aging Cell 2018 May 28:e12778. Epub 2018 May 28.
Department of Integrative Biology and Physiology, University of Minnesota, Minneapolis, Minnesota.
Stress and low socioeconomic status in humans confer increased vulnerability to morbidity and mortality. However, this association is not mechanistically understood nor has its causation been explored in animal models thus far. Recently, cellular senescence has been suggested as a potential mechanism linking lifelong stress to age-related diseases and shorter life expectancy in humans. Read More
Aging Cell 2018 May 27:e12786. Epub 2018 May 27.
Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan.
Longevity in mammals is influenced by sex, and lifespan extension in response to anti-aging interventions is often sex-specific, although the mechanisms underlying these sexual dimorphisms are largely unknown. Treatment of mice with 17-α estradiol (17aE2) results in sex-specific lifespan extension, with an increase in median survival in males of 19% and no survival effect in females. Given the links between lifespan extension and metabolism, we performed untargeted metabolomics analysis of liver, skeletal muscle and plasma from male and female mice treated with 17aE2 for eight months. Read More
Aging Cell 2018 May 24:e12785. Epub 2018 May 24.
Laboratory of Epidemiology and Population Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland.
Circulating extracellular RNAs (exRNAs) are potential biomarkers of disease. We thus hypothesized that age-related changes in exRNAs can identify age-related processes. We profiled both large and small RNAs in human serum to investigate changes associated with normal aging. Read More
Aging Cell 2018 May 23:e12779. Epub 2018 May 23.
Biodemography of Aging Research Unit, Social Science Research Institute, Duke University, Durham, North Carolina.
Although the APOE region is the strongest genetic risk factor for Alzheimer's diseases (ADs), its pathogenic role remains poorly understood. Elucidating genetic predisposition to ADs, a subset of age-related diseases characteristic for postreproductive period, is hampered by the undefined role of evolution in establishing molecular mechanisms of such diseases. This uncertainty is inevitable source of natural-selection-free genetic heterogeneity in predisposition to ADs. Read More
Aging Cell 2018 May 17:e12783. Epub 2018 May 17.
Department of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut.
Coats plus (CP) is a rare autosomal recessive disorder caused by mutations in CTC1, a component of the CST (CTC1, STN1, and TEN1) complex important for telomere length maintenance. The molecular basis of how CP mutations impact upon telomere length remains unclear. The CP CTC1 mutation has been previously shown to disrupt telomere maintenance. Read More
Aging Cell 2018 May 17:e12761. Epub 2018 May 17.
Department of Surgery, College of Medicine, University of Florida, Gainesville, FL, USA.
Ischemia/reperfusion (I/R) injury is a causative factor contributing to morbidity and mortality during liver resection and transplantation. Livers from elderly patients have a poorer recovery from these surgeries, indicating reduced reparative capacity with aging. Mechanisms underlying this age-mediated hypersensitivity to I/R injury remain poorly understood. Read More
Aging Cell 2018 May 15:e12780. Epub 2018 May 15.
Department of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
The selective depletion of senescent cells (SCs) by small molecules, termed senolytic agents, is a promising therapeutic approach for treating age-related diseases and chemotherapy- and radiotherapy-induced side effects. Piperlongumine (PL) was recently identified as a novel senolytic agent. However, its mechanism of action and molecular targets in SCs was unknown and thus was investigated. Read More
Aging Cell 2018 May 10:e12768. Epub 2018 May 10.
Department of Geriatrics, Fujian Medical University Union Hospital, Fuzhou, China.
Gut microbiota can influence the aging process and may modulate aging-related changes in cognitive function. Trimethylamine-N-oxide (TMAO), a metabolite of intestinal flora, has been shown to be closely associated with cardiovascular disease and other diseases. However, the relationship between TMAO and aging, especially brain aging, has not been fully elucidated. Read More
Aging Cell 2018 May 10:e12775. Epub 2018 May 10.
Arizona State University-Banner Neurodegenerative Disease Research Center at the Biodesign Institute, Arizona State University, Tempe, AZ, USA.
Misfolded and hyperphosphorylated tau accumulates in several neurodegenerative disorders including Alzheimer's disease, frontotemporal dementia with Parkinsonism, corticobasal degeneration, progressive supranuclear palsy, Down syndrome, and Pick's disease. Tau is a microtubule-binding protein, and its role in microtubule stabilization is well defined. In contrast, while growing evidence suggests that tau is also involved in synaptic physiology, a complete assessment of tau function in the adult brain has been hampered by robust developmental compensation of other microtubule-binding proteins in tau knockout mice. Read More
Aging Cell 2018 May 9:e12773. Epub 2018 May 9.
Division of Cardiovascular Medicine, University of Cambridge, Cambridge, UK.
Aging is the largest risk factor for cardiovascular disease, yet the molecular mechanisms underlying vascular aging remain unclear. Mitochondrial DNA (mtDNA) damage is linked to aging, but whether mtDNA damage or mitochondrial dysfunction is present and directly promotes vascular aging is unknown. Furthermore, mechanistic studies in mice are severely hampered by long study times and lack of sensitive, repeatable and reproducible parameters of arterial aging at standardized early time points. Read More
Aging Cell 2018 May 9:e12771. Epub 2018 May 9.
Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina.
Cellular senescence drives a functional decline of numerous tissues with aging by limiting regenerative proliferation and/or by producing pro-inflammatory molecules known as the senescence-associated secretory phenotype (SASP). The senescence biomarker p16 is a potent inhibitor of the cell cycle but is not essential for SASP production. Thus, it is unclear whether p16 identifies senescence in hyporeplicative cells such as articular chondrocytes and whether p16 contributes to pathologic characteristics of cartilage aging. Read More
Aging Cell 2018 May 8:e12774. Epub 2018 May 8.
Neuroprotective Drug Discovery Key Laboratory of Nanjing Medical University, Nanjing, Jiangsu, China.
Microglia-mediated neuroinflammation plays a dual role in various brain diseases due to distinct microglial phenotypes, including deleterious M1 and neuroprotective M2. There is growing evidence that the peroxisome proliferator-activated receptor γ (PPARγ) agonist rosiglitazone prevents lipopolysaccharide (LPS)-induced microglial activation. Here, we observed that antagonizing PPARγ promoted LPS-stimulated changes in polarization from the M1 to the M2 phenotype in primary microglia. Read More
Aging Cell 2018 May 8:e12772. Epub 2018 May 8.
ProCURE (Program Against Cancer Therapeutic Resistance), Metabolism & Cancer Group, Catalan Institute of Oncology, Girona, Catalonia, Spain.
Metformin, the first drug chosen to be tested in a clinical trial aimed to target the biology of aging per se, has been clinically exploited for decades in the absence of a complete understanding of its therapeutic targets or chemical determinants. We here outline a systematic chemoinformatics approach to computationally predict biomolecular targets of metformin. Using several structure- and ligand-based software tools and reference databases containing 1,300,000 chemical compounds and more than 9,000 binding sites protein cavities, we identified 41 putative metformin targets including several epigenetic modifiers such as the member of the H3K27me3-specific demethylase subfamily, KDM6A/UTX. Read More
Aging Cell 2018 May 5:e12710. Epub 2018 May 5.
Edward S. Harkness Eye Institute, New York-Presbyterian Hospital, New York, NY, USA.
High-temperature requirement protein A1 (HTRA1) is a serine protease secreted by a number of tissues including retinal pigment epithelium (RPE). A promoter variant of the gene encoding HTRA1 is part of a mutant allele that causes increased HTRA1 expression and contributed to age-related macular degeneration (AMD) in genomewide association studies. AMD is characterized by pathological development of drusen, extracellular deposits of proteins and lipids on the basal side of RPE. Read More
Aging Cell 2018 Apr 28:e12767. Epub 2018 Apr 28.
Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Calorie restriction (CR) is one of the most robust means to improve health and survival in model organisms. CR imposes a metabolic program that leads to increased stress resistance and delayed onset of chronic diseases, including cancer. In rodents, CR induces the upregulation of two NADH-dehydrogenases, namely NAD(P)H:quinone oxidoreductase 1 (Nqo1) and cytochrome b reductase 3 (Cyb5r3), which provide electrons for energy metabolism. Read More
Aging Cell 2018 Apr 25:e12769. Epub 2018 Apr 25.
Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma.
Loss of SURF1, a Complex IV assembly protein, was reported to increase lifespan in mice despite dramatically lower cytochrome oxidase (COX) activity. Consistent with this, our previous studies found advantageous changes in metabolism (reduced adiposity, increased insulin sensitivity, and mitochondrial biogenesis) in Surf1 mice. The lack of deleterious phenotypes in Surf1 mice is contrary to the hypothesis that mitochondrial dysfunction contributes to aging. Read More
Aging Cell 2018 Apr 25:e12770. Epub 2018 Apr 25.
Department of Geriatric Medicine, Oklahoma University Health Science Center, Oklahoma City, OK, USA.
Necroptosis is a newly identified programmed cell death pathway that is highly proinflammatory due to the release of cellular components that promote inflammation. To determine whether necroptosis might play a role in inflammaging, we studied the effect of age and dietary restriction (DR) on necroptosis in the epididymal white adipose tissue (eWAT), a major source of proinflammatory cytokines. Phosphorylated MLKL and RIPK3, markers of necroptosis, were increased 2. Read More
Aging Cell 2018 Apr 25:e12766. Epub 2018 Apr 25.
Aix Marseille Univ, INSERM, MMG, Marseille, France.
Hereditary and sporadic laminopathies are caused by mutations in genes encoding lamins, their partners, or the metalloprotease ZMPSTE24/FACE1. Depending on the clinical phenotype, they are classified as tissue-specific or systemic diseases. The latter mostly manifest with several accelerated aging features, as in Hutchinson-Gilford progeria syndrome (HGPS) and other progeroid syndromes. Read More
Aging Cell 2018 Apr 19:e12740. Epub 2018 Apr 19.
Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Lifespan varies dramatically among species, but the biological basis is not well understood. Previous studies in model organisms revealed the importance of nutrient sensing, mTOR, NAD/sirtuins, and insulin/IGF1 signaling in lifespan control. By studying life-history traits and transcriptomes of 14 Drosophila species differing more than sixfold in lifespan, we explored expression divergence and identified genes and processes that correlate with longevity. Read More
Aging Cell 2018 Apr 16:e12765. Epub 2018 Apr 16.
National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Metformin, an FDA-approved antidiabetic drug, has been shown to elongate lifespan in animal models. Nevertheless, the effects of metformin on human cells remain unclear. Here, we show that low-dose metformin treatment extends the lifespan of human diploid fibroblasts and mesenchymal stem cells. Read More
Aging Cell 2018 Apr 16:e12762. Epub 2018 Apr 16.
Department of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
DNA methylation increases with age. The objective of this study was to investigate whether compound H, a potential activator of DNA demethylases, attenuates aging-related arterial stiffness and hypertension. Aged mice (24-27 months) and adult mice (12 months) were used. Read More
Aging Cell 2018 Apr 16:e12764. Epub 2018 Apr 16.
Department of Spinal Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Osteoblast apoptosis contributes to age-related bone loss. Advanced oxidation protein products (AOPPs) are recognized as the markers of oxidative stress and potent inducers of apoptosis. We have demonstrated that AOPP accumulation was correlated with age-related bone loss. Read More
Aging Cell 2018 Apr 16:e12763. Epub 2018 Apr 16.
Division of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Lipotoxicity cardiomyopathy is the result of excessive accumulation and oxidation of toxic lipids in the heart. It is a major threat to patients with diabetes. Glucagon-like peptide-1 (GLP-1) has aroused considerable interest as a novel therapeutic target for diabetes mellitus because it stimulates insulin secretion. Read More
Aging Cell 2018 Apr 14:e12751. Epub 2018 Apr 14.
Department of Cell Biology & Molecular Medicine, Rutgers University-New Jersey Medical School, Newark, NJ, USA.
Disruption of the regulator for G protein signaling 14 (RGS14) knockout (KO) in mice extends their lifespan and has multiple beneficial effects related to healthful aging, that is, protection from obesity, as reflected by reduced white adipose tissue, protection against cold exposure, and improved metabolism. The observed beneficial effects were mediated by improved mitochondrial function. But most importantly, the main mechanism responsible for the salutary properties of the RGS14 KO involved an increase in brown adipose tissue (BAT), which was confirmed by surgical BAT removal and transplantation to wild-type (WT) mice, a surgical simulation of a molecular knockout. Read More
Aging Cell 2018 Apr 10:e12730. Epub 2018 Apr 10.
Dipartimento di Biologia e Biotecnologie "C. Darwin", Sapienza Università di Roma, Rome, Italy.
Human AKTIP and mouse Ft1 are orthologous ubiquitin E2 variant proteins involved in telomere maintenance and DNA replication. AKTIP also interacts with A- and B-type lamins. These features suggest that Ft1 may be implicated in aging regulatory pathways. Read More
Aging Cell 2018 Apr 6:e12760. Epub 2018 Apr 6.
Department of Molecular Neurobiology, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
A proper equilibrium of post-translational protein modifications is essential for normal cell physiology, and alteration in these processes is key in neurodegenerative disorders such as Alzheimer's disease. Recently, for instance, alteration in protein SUMOylation has been linked to amyloid pathology. In this work, we aimed to elucidate the role of protein SUMOylation during aging and increased amyloid burden in vivo using a His -HA-SUMO1 knock-in mouse in the 5XFAD model of Alzheimer's disease. Read More
Aging Cell 2018 Jun 1;17(3):e12759. Epub 2018 Apr 1.
Alzheimer's Center at Temple, Lewis Katz Temple University School of Medicine, Philadelphia, PA, USA.
The 5-lipoxygenase (5LO) is a source of inflammatory leukotrienes and is upregulated in Alzheimer's disease and related tauopathies. However, whether it directly modulates tau phosphorylation and the development of its typical neuropathology in the absence of Aβ or is a secondary event during the course of the disease pathogenesis remains to be fully elucidated. The goal of this study was to evaluate the effect that pharmacologic blockade of this inflammatory pathway has on the phenotype of a transgenic mouse model of tauopathy, the P301S mice. Read More
Aging Cell 2018 Jun 30;17(3):e12748. Epub 2018 Mar 30.
Division of Physiology, Department of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA, USA.
Aortic stiffening is an independent risk factor that underlies cardiovascular morbidity in the elderly. We have previously shown that intrinsic mechanical properties of vascular smooth muscle cells (VSMCs) play a key role in aortic stiffening in both aging and hypertension. Here, we test the hypothesis that VSMCs also contribute to aortic stiffening through their extracellular effects. Read More
Aging Cell 2018 Jun 30;17(3):e12758. Epub 2018 Mar 30.
Department of Orthopedics, Chinese PLA General Hospital, Beijing, China.
Exosomes are secreted into the blood by various types of cells. These extracellular vesicles are involved in the contribution of exosomal proteins to osteoblastic or osteoclastic regulatory networks during the failure of bone remodeling, which results in age-related bone loss. However, the molecular changes in serum-derived exosomes (SDEs) from aged patients with low bone density and their functions in bone remodeling remain to be fully elucidated. Read More
Aging Cell 2018 Jun 25;17(3):e12754. Epub 2018 Mar 25.
Department of Pharmacology, Nanjing Medical University, Nanjing, China.
In neurons, increased protein-protein interactions between neuronal nitric oxide synthase (nNOS) and its carboxy-terminal PDZ ligand (CAPON) contribute to excitotoxicity and abnormal dendritic spine development, both of which are involved in the development of Alzheimer's disease. In models of Alzheimer's disease, increased nNOS-CAPON interaction was detected after treatment with amyloid-β in vitro, and a similar change was found in the hippocampus of APP/PS1 mice (a transgenic mouse model of Alzheimer's disease), compared with age-matched background mice in vivo. After blocking the nNOS-CAPON interaction, memory was rescued in 4-month-old APP/PS1 mice, and dendritic impairments were ameliorated both in vivo and in vitro. Read More
Aging Cell 2018 Jun 25;17(3):e12755. Epub 2018 Mar 25.
Department of Biology, Ecology and Earth Sciences, University of Calabria, Rende, Italy.
In human longevity studies, single nucleotide polymorphism (SNP) analysis identified a large number of genetic variants with small effects, yet not easily replicable in different populations. New insights may come from the combined analysis of different SNPs, especially when grouped by metabolic pathway. We applied this approach to study the joint effect on longevity of SNPs belonging to three candidate pathways, the insulin/insulin-like growth factor signalling (IIS), DNA repair and pro/antioxidant. Read More
Aging Cell 2018 Jun 24;17(3):e12756. Epub 2018 Mar 24.
Program in Metabolic Biology, Nutritional Sciences & Toxicology, University of California, Berkeley, CA, USA.
The mitochondrial unfolded protein response (UPR ), a cellular protective program that ensures proteostasis in the mitochondria, has recently emerged as a regulatory mechanism for adult stem cell maintenance that is conserved across tissues. Despite the emerging genetic evidence implicating the UPR in stem cell maintenance, the underlying molecular mechanism is unknown. While it has been speculated that the UPR is activated upon stem cell transition from quiescence to proliferation, the direct evidence is lacking. Read More
Aging Cell 2018 Jun 24;17(3):e12752. Epub 2018 Mar 24.
Bone and Joint Research Center, The First Affiliated Hospital and Frontier Institute of Science and Technology, Xi'an JiaoTong University, Xi'an, China.
Primary osteoarthritis (OA) is associated with aging, while post-traumatic OA (PTOA) is associated with mechanical injury and inflammation. It is not clear whether the two types of osteoarthritis share common mechanisms. We found that miR-146a, a microRNA-associated with inflammation, is activated by cyclic load in the physiological range but suppressed by mechanical overload in human articular chondrocytes. Read More
Aging Cell 2018 Jun 25;17(3):e12749. Epub 2018 Mar 25.
Unidad de Genómica Avanzada (Langebio), Centro de Investigación y de Estudios Avanzados del IPN, Irapuato, Guanajuato, Mexico.
Dietary restriction is arguably the most promising nonpharmacological intervention to extend human life and health span. Yet, only few genetic regulators mediating the cellular response to dietary restriction are known, and the question remains which other regulatory factors are involved. Here, we measured at the genomewide level the chronological lifespan of Saccharomyces cerevisiae gene deletion strains under two nitrogen source regimens, glutamine (nonrestricted) and γ-aminobutyric acid (restricted). Read More
Aging Cell 2018 Jun 25;17(3):e12738. Epub 2018 Mar 25.
Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Aging is characterized by numerous molecular changes, such as accumulation of molecular damage and altered gene expression, many of which are linked to DNA methylation. Here, we characterize the blood DNA methylome across 16 age groups of mice and report numerous global, region- and site-specific features, as well as the associated dynamics of methylation changes. Transition of the methylome throughout lifespan was not uniform, with many sites showing accelerated changes in late life. Read More
Aging Cell 2018 Jun 25;17(3):e12747. Epub 2018 Mar 25.
Department of Biology, Molecular Biology and Heart Institutes, San Diego State University, San Diego, CA, USA.
Mutations in the human LMNA gene cause a collection of diseases known as laminopathies. These include myocardial diseases that exhibit age-dependent penetrance of dysrhythmias and heart failure. The LMNA gene encodes A-type lamins, intermediate filaments that support nuclear structure and organize the genome. Read More
Aging Cell 2018 Jun 25;17(3):e12746. Epub 2018 Mar 25.
European Research Institute for the Biology of Aging, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Calorie restriction (CR) is an effective strategy to delay the onset and progression of aging phenotypes in a variety of organisms. Several molecular players are involved in the anti-aging effects of CR, but mechanisms of regulation are poorly understood. Cellular senescence-a cellular state of irreversible growth arrest-is considered a basic mechanism of aging. Read More
Aging Cell 2018 Jun 24;17(3):e12757. Epub 2018 Mar 24.
Department of Genetics, Stanford University, Stanford, CA, USA.
The African turquoise killifish has recently gained significant traction as a new research organism in the aging field. Our understanding of aging has strongly benefited from canonical research organisms-yeast, C. elegans, Drosophila, zebrafish, and mice. Read More