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Mitochondria AND aging

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https://www.readbyqxmd.com/read/28649426/conserved-and-species-specific-molecular-denominators-in-mammalian-skeletal-muscle-aging
#1
Evi M Mercken, Miriam Capri, Bethany A Carboneau, Maria Conte, Juliana Heidler, Aurelia Santoro, Alejandro Martin-Montalvo, Marta Gonzalez-Freire, Husam Khraiwesh, José A González-Reyes, Ruin Moaddel, Yongqing Zhang, Kevin G Becker, José M Villalba, Julie A Mattison, Ilka Wittig, Claudio Franceschi, Rafael de Cabo
Aging is a complex phenomenon involving functional decline in multiple physiological systems. We undertook a comparative analysis of skeletal muscle from four different species, i.e. mice, rats, rhesus monkeys, and humans, at three different representative stages during their lifespan (young, middle, and old) to identify pathways that modulate function and healthspan. Gene expression profiling and computational analysis revealed that pathway complexity increases from mice to humans, and as mammals age, there is predominantly an upregulation of pathways in all species...
2017: NPJ Aging and Mechanisms of Disease
https://www.readbyqxmd.com/read/28649287/regulating-role-of-fetal-thyroid-hormones-on-placental-mitochondrial-dna-methylation-epidemiological-evidence-from-the-environage-birth-cohort-study
#2
Bram G Janssen, Hyang-Min Byun, Harry A Roels, Wilfried Gyselaers, Joris Penders, Andrea A Baccarelli, Tim S Nawrot
BACKGROUND: Fetal development largely depends on thyroid hormone availability and proper placental function with an important role played by placental mitochondria. The biological mechanisms by which thyroid hormones exert their effects on mitochondrial function are not well understood. We investigated the role of fetal thyroid hormones on placental mitochondrial DNA (mtDNA) content and mtDNA methylation. We collected placental tissue and cord blood from 305 mother-child pairs that were enrolled between February 2010 and June 2014 in the ENVIRONAGE (ENVIRonmental influence ON early AGEing) birth cohort (province of Limburg, Belgium)...
2017: Clinical Epigenetics
https://www.readbyqxmd.com/read/28649097/-aging-and-homeostasis-aging-of-skeletal-muscle
#3
Ruriko Suzuki, Yoshifumi Tamura
With aging, insulin resistance and sarcopenia in skeletal muscle are induced, resulting in skeletal muscle aging. It is suggested that the former is one of the reasons that mitochondrial function decreases with aging, and the latter is due to endocrinologic dysfunction, neurological mechanism, nutritional deficiency and inactivity such as waste are complicatedly involved. Also, as sarcopenia progresses, the amount of physical activity further decreases, and it is also assumed that insulin resistance and sarcopenia progress synergistically...
2017: Clinical Calcium
https://www.readbyqxmd.com/read/28645153/defective-mitochondrial-rna-processing-due-to-pnpt1-variants-causes-leigh-syndrome
#4
Sanna Matilainen, Christopher J Carroll, Uwe Richter, Liliya Euro, Max Pohjanpelto, Anders Paetau, Pirjo Isohanni, Anu Suomalainen
Leigh syndrome is a severe infantile encephalopathy with an exceptionally variable genetic background. We studied the exome of a child manifesting with Leigh syndrome at one month of age and progressing to death by the age of 2.4 years, and identified novel compound heterozygous variants in PNPT1, encoding the polynucleotide phosphorylase (PNPase). Expression of the wild type PNPT1 in the subject's myoblasts functionally complemented the defects, and the pathogenicity was further supported by structural predictions and protein and RNA analyses...
June 22, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28644888/fragmentation-of-the-mitochondrial-network-in-skin-in-vivo
#5
Daniel Mellem, Martin Sattler, Sonja Pagel-Wolff, Sören Jaspers, Horst Wenck, Michael Alexander Rübhausen, Frank Fischer
Mitochondria form dynamic networks which adapt to the environmental requirements of the cell. We investigated the aging process of these networks in human skin cells in vivo by multiphoton microscopy. A study on the age-dependency of the mitochondrial network in young and old volunteers revealed that keratinocytes in old skin establish a significantly more fragmented network with smaller and more compact mitochondrial clusters than keratinocytes in young skin. Furthermore, we investigated the mitochondrial network during differentiation processes of keratinocytes within the epidermis of volunteers...
2017: PloS One
https://www.readbyqxmd.com/read/28644434/ageing-and-hypoxia-cause-protein-aggregation-in-mitochondria
#6
Daniel M Kaufman, Xia Wu, Barbara A Scott, Omar A Itani, Marc R Van Gilst, James E Bruce, C Michael Crowder
Aggregation of cytosolic proteins is a pathological finding in disease states, including ageing and neurodegenerative diseases. We have previously reported that hypoxia induces protein misfolding in Caenorhabditis elegans mitochondria, and electron micrographs suggested protein aggregates. Here, we seek to determine whether mitochondrial proteins actually aggregate after hypoxia and other cellular stresses. To enrich for mitochondrial proteins that might aggregate, we performed a proteomics analysis on purified C...
June 23, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28641368/glomerular-hyperfiltration-in-obese-african-american-hypertensive-patients-is-associated-with-elevated-urinary-mitochondrial-dna-copy-number
#7
Alfonso Eirin, Ahmed Saad, John R Woollard, Luis A Juncos, David A Calhoun, Hui Tang, Amir Lerman, Stephen C Textor, Lilach O Lerman
BACKGROUND: Glomerular hyperfiltration may contribute to the high incidence of renal disease in Obese African Americans essential hypertensive (ObAAEH) patients, but the precise mechanisms responsible for renal injury have not been elucidated. Mitochondria are important determinants of renal injury in hypertension, and increased levels of mitochondrial DNA (mtDNA) in the urine may indicate renal mitochondrial injury. We hypothesized that urine mtDNA copy numbers would be higher in ObAAEH compared to Caucasian essential hypertensive (CEH) patients...
June 14, 2017: American Journal of Hypertension
https://www.readbyqxmd.com/read/28640253/a-role-for-tspo-in-mitochondrial-ca-2-homeostasis-and-redox-stress-signaling
#8
Jemma Gatliff, Daniel A East, Aarti Singh, Maria Soledad Alvarez, Michele Frison, Ivana Matic, Caterina Ferraina, Natalie Sampson, Federico Turkheimer, Michelangelo Campanella
The 18 kDa translocator protein TSPO localizes on the outer mitochondrial membrane (OMM). Systematically overexpressed at sites of neuroinflammation it is adopted as a biomarker of brain conditions. TSPO inhibits the autophagic removal of mitochondria by limiting PARK2-mediated mitochondrial ubiquitination via a peri-organelle accumulation of reactive oxygen species (ROS). Here we describe that TSPO deregulates mitochondrial Ca(2+) signaling leading to a parallel increase in the cytosolic Ca(2+) pools that activate the Ca(2+)-dependent NADPH oxidase (NOX) thereby increasing ROS...
June 22, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28638045/treatment-of-sarcopenia-and-glucose-intolerance-through-mitochondrial-activation-by-5-aminolevulinic-acid
#9
Chikako Fujii, Kazutoshi Miyashita, Masanori Mitsuishi, Masaaki Sato, Kentaro Fujii, Hiroyuki Inoue, Aika Hagiwara, Sho Endo, Asuka Uto, Masaki Ryuzaki, Motowo Nakajima, Tohru Tanaka, Masanori Tamaki, Ayako Muraki, Toshihide Kawai, Hiroshi Itoh
Recently, sarcopenia has attracted attention as therapeutic target because it constitutes a risk factor for metabolic and cardiovascular diseases. We focused 5-aminolevulinic acid (ALA) which act as electron carriers in the mitochondrial electron transport system. The mice that received ALA for 8 weeks gained muscle strength and endurance, and exhibited increased muscle mass and mitochondrial amount. Administration of ALA to sarcopenia mice aged 100 weeks and chronic kidney disease (CKD) model mice also increased muscle mass and improved physical performance...
June 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28637402/antioxidant-skq1-alleviates-signs-of-alzheimer-s-disease-like-pathology-in-old-oxys-rats-by-reversing-mitochondrial-deterioration
#10
Nataliya G Kolosova, Mikhail A Tyumentsev, Natalia A Muraleva, Elena Kiseleva, Anton O Vitovtov, Natalia A Stefanova
BACKGROUND: Mitochondrial dysfunction is called the missing link between brain aging and Alzheimer's disease (AD), the most common type of age-related dementia worldwide. Among the most advanced and promising of approaches to prevention or slowing of AD are therapeutic strategies targeting mitochondria. OBJECTIVE: Mitochondria-targeted antioxidant SkQ1 can suppress the development of AD signs, but its therapeutic potential in AD at clinical stages is currently unknown...
June 21, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28626500/mitophagy-transcriptome-mechanistic-insights-into-polyphenol-mediated-mitophagy
#11
REVIEW
Sijie Tan, Esther Wong
Mitochondria are important bioenergetic and signalling hubs critical for myriad cellular functions and homeostasis. Dysfunction in mitochondria is a central theme in aging and diseases. Mitophagy, a process whereby damaged mitochondria are selectively removed by autophagy, plays a key homeostatic role in mitochondrial quality control. Upregulation of mitophagy has shown to mitigate superfluous mitochondrial accumulation and toxicity to safeguard mitochondrial fitness. Hence, mitophagy is a viable target to promote longevity and prevent age-related pathologies...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28622510/microbial-genetic-composition-tunes-host-longevity
#12
Bing Han, Priya Sivaramakrishnan, Chih-Chun J Lin, Isaiah A A Neve, Jingquan He, Li Wei Rachel Tay, Jessica N Sowa, Antons Sizovs, Guangwei Du, Jin Wang, Christophe Herman, Meng C Wang
Homeostasis of the gut microbiota critically influences host health and aging. Developing genetically engineered probiotics holds great promise as a new therapeutic paradigm to promote healthy aging. Here, through screening 3,983 Escherichia coli mutants, we discovered that 29 bacterial genes, when deleted, increase longevity in the host Caenorhabditis elegans. A dozen of these bacterial mutants also protect the host from age-related progression of tumor growth and amyloid-beta accumulation. Mechanistically, we discovered that five bacterial mutants promote longevity through increased secretion of the polysaccharide colanic acid (CA), which regulates mitochondrial dynamics and unfolded protein response (UPR(mt)) in the host...
June 15, 2017: Cell
https://www.readbyqxmd.com/read/28622501/microbiome-and-longevity-gut-microbes-send-signals-to-host-mitochondria
#13
Jan Gruber, Brian K Kennedy
The microbiome has emerged as a major determinant of the functioning of host organisms, affecting both health and disease. Here, Han et al. use the workhorse of aging research, C. elegans, to identify specific mechanisms by which gut bacteria influence mitochondrial dynamics and aging, a first step toward analogous manipulations to modulate human aging.
June 15, 2017: Cell
https://www.readbyqxmd.com/read/28619690/metformin-the-aspirin-of-the-21-st-century-its-role-in-gestational-diabetes-prevention-of-preeclampsia-and-cancer-and-the-promotion-of-longevity
#14
REVIEW
Roberto Romero, Offer Erez, Maik Hüttemann, Eli Maymon, Bogdan Panaitescu, Agustin Conde-Agudelo, Percy Pacora, Bo Hyun Yoon, Lawrence I Grossman
Metformin is everywhere. Originally introduced in clinical practice as an anti-diabetic agent, its role as a therapeutic agent is expanding to include treatment of pre-diabetes, gestational diabetes, polycystic ovarian disease, and more recently, experimental studies, as well as observations in randomized clinical trials, suggest that metformin could have a place in the treatment or prevention of preeclampsia. This article provides a brief overview of the history of metformin in the treatment of diabetes, reviews the results of meta-analyses of metformin in gestational diabetes, and the treatment of obese non-diabetic pregnant women to prevent macrosomia...
June 12, 2017: American Journal of Obstetrics and Gynecology
https://www.readbyqxmd.com/read/28619096/presenilins-regulate-synaptic-plasticity-and-mitochondrial-calcium-homeostasis-in-the-hippocampal-mossy-fiber-pathway
#15
Sang Hun Lee, David Lutz, Mohanad Mossalam, Vadim Y Bolshakov, Michael Frotscher, Jie Shen
BACKGROUND: Presenilins play a major role in the pathogenesis of Alzheimer's disease, in which the hippocampus is particularly vulnerable. Previous studies of Presenilin function in the synapse, however, focused exclusively on the hippocampal Schaffer collateral (SC) pathway. Whether Presenilins play similar or distinct roles in other hippocampal synapses is unknown. METHODS: To investigate the role of Presenilins at mossy fiber (MF) synapses we performed field and whole-cell electrophysiological recordings and Ca(2+) imaging using acute hippocampal slices of postnatal forebrain-restricted Presenilin conditional double knockout (PS cDKO) and control mice at 2 months of age...
June 15, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28618992/modulating-mitophagy-in-mitochondrial-disease
#16
Eszter Dombi, Heather Mortiboys, Joanna Poulton
Mitochondrial diseases may result from mutations in the maternally-inherited mitochondrial DNA (mtDNA) or from mutations in nuclear genes encoding mitochondrial proteins. Their bi-genomic nature makes mitochondrial diseases a very heterogeneous group of disorders that can present at any age and can affect any type of tissue. The autophagic-lysosomal degradation pathway plays an important role in clearing dysfunctional and redundant mitochondria through a specific quality control mechanism termed mitophagy. Mitochondria could be targeted for autophagic degradation for a variety of reasons including basal turnover for recycling, starvation induced degradation, and degradation due to damage...
June 16, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28614723/single-muscle-fiber-proteomics-reveals-fiber-type-specific-features-of-human-muscle-aging
#17
Marta Murgia, Luana Toniolo, Nagarjuna Nagaraj, Stefano Ciciliot, Vincenzo Vindigni, Stefano Schiaffino, Carlo Reggiani, Matthias Mann
Skeletal muscle is a key tissue in human aging, which affects different muscle fiber types unequally. We developed a highly sensitive single muscle fiber proteomics workflow to study human aging and show that the senescence of slow and fast muscle fibers is characterized by diverging metabolic and protein quality control adaptations. Whereas mitochondrial content declines with aging in both fiber types, glycolysis and glycogen metabolism are upregulated in slow but downregulated in fast muscle fibers. Aging mitochondria decrease expression of the redox enzyme monoamine oxidase A...
June 13, 2017: Cell Reports
https://www.readbyqxmd.com/read/28612522/-the-mechanisms-of-trimetazidine-alleviating-the-oxidative-stress-in-adipose-derived-mesenchymal-stem-cells
#18
Mao-Han Tang, Yan-Jie Zhang, Yin Liu, Zhi-Guang Su
OBJECTIVES: To investigate the effects of trimetazidine (TMZ) on the oxidative stress injury in adipose-derived mesenchymal stem cells (ADSCs). METHODS: ADSCs derived from adipose tissue of SD rats were characterized by flow cytometry and multiline age differentiation. ADSCs apoptosis was induced by H2O2 in vitro , Dirrerent concentration of TMZ (250 μmol/L, 500 μmol/L) was used to protect ADSCs from apoptosis. The morphological features of apoptotic ADSCs were analyzed by Hoechst 33342, mitochondrial potential and structure was analyzed by JC-1 staining and electron microscope, respectively...
March 2017: Sichuan da Xue Xue Bao. Yi Xue Ban, Journal of Sichuan University. Medical Science Edition
https://www.readbyqxmd.com/read/28611589/mitochondrial-effects-of-pgc-1alpha-silencing-in-mpp-treated-human-sh-sy5y-neuroblastoma-cells
#19
Qinyong Ye, Chun Chen, Erwang Si, Yousheng Cai, Juhua Wang, Wanling Huang, Dongzhu Li, Yingqing Wang, Xiaochun Chen
The dopaminergic neuron degeneration and loss that occurs in Parkinson's disease (PD) has been tightly linked to mitochondrial dysfunction. Although the aged-related cause of the mitochondrial defect observed in PD patients remains unclear, nuclear genes are of potential importance to mitochondrial function. Human peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) is a multi-functional transcription factor that tightly regulates mitochondrial biogenesis and oxidative capacity. The goal of the present study was to explore the potential pathogenic effects of interference by the PGC-1α gene on N-methyl-4-phenylpyridinium ion (MPP(+))-induced SH-SY5Y cells...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28608850/cellular-senescence-drives-age-dependent-hepatic-steatosis
#20
Mikolaj Ogrodnik, Satomi Miwa, Tamar Tchkonia, Dina Tiniakos, Caroline L Wilson, Albert Lahat, Christoper P Day, Alastair Burt, Allyson Palmer, Quentin M Anstee, Sushma Nagaraja Grellscheid, Jan H J Hoeijmakers, Sander Barnhoorn, Derek A Mann, Thomas G Bird, Wilbert P Vermeij, James L Kirkland, João F Passos, Thomas von Zglinicki, Diana Jurk
The incidence of non-alcoholic fatty liver disease (NAFLD) increases with age. Cellular senescence refers to a state of irreversible cell-cycle arrest combined with the secretion of proinflammatory cytokines and mitochondrial dysfunction. Senescent cells contribute to age-related tissue degeneration. Here we show that the accumulation of senescent cells promotes hepatic fat accumulation and steatosis. We report a close correlation between hepatic fat accumulation and markers of hepatocyte senescence. The elimination of senescent cells by suicide gene-meditated ablation of p16(Ink4a)-expressing senescent cells in INK-ATTAC mice or by treatment with a combination of the senolytic drugs dasatinib and quercetin (D+Q) reduces overall hepatic steatosis...
June 13, 2017: Nature Communications
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