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Mitochondria AND aging

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https://www.readbyqxmd.com/read/29049454/association-of-mitochondrial-dna-copy-number-with-cardiovascular-disease
#1
Foram N Ashar, Yiyi Zhang, Ryan J Longchamps, John Lane, Anna Moes, Megan L Grove, Josyf C Mychaleckyj, Kent D Taylor, Josef Coresh, Jerome I Rotter, Eric Boerwinkle, Nathan Pankratz, Eliseo Guallar, Dan E Arking
Importance: Mitochondrial dysfunction is a core component of the aging process and may play a key role in atherosclerotic cardiovascular disease. Mitochondrial DNA copy number (mtDNA-CN), which represents the number of mitochondria per cell and number of mitochondrial genomes per mitochondrion, is an indirect biomarker of mitochondrial function. Objective: To determine whether mtDNA-CN, measured in an easily accessible tissue (buffy coat/circulating leukocytes), can improve risk classification for cardiovascular disease (CVD) and help guide initiation of statin therapy for primary prevention of CVD...
October 11, 2017: JAMA Cardiology
https://www.readbyqxmd.com/read/29047092/redox-signaling-and-persistent-pulmonary-hypertension-of-the-newborn
#2
Megha Sharma, Adeleye J Afolayan
Reactive oxygen species (ROS) are redox-signaling molecules that are critically involved in regulating endothelial cell functions, host defense, aging, and cellular adaptation. Mitochondria are the major sources of ROS and important sources of redox signaling in pulmonary circulation. It is becoming increasingly evident that increased mitochondrial oxidative stress and aberrant signaling through redox-sensitive pathways play a direct causative role in the pathogenesis of many cardiopulmonary disorders including persistent pulmonary hypertension of the newborn (PPHN)...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/29045673/age-related-changes-in-the-mitochondria-of-human-mural-granulosa-cells
#3
Yifan Liu, Ming Han, Xiaoshuang Li, Hui Wang, Minyue Ma, Shihui Zhang, Yifan Guo, Shuling Wang, Yuanfen Wang, N Duan, Bing Xu, Jingwen Yin, Yuanqing Yao
STUDY QUESTION: What changes in the mitochondria of human mural granulosa cells (mGCs) with maternal aging? SUMMARY ANSWER: The mitochondrial membrane potential (MMP) and the ability of oxidative phosphorylation (OXPHOS) of mGCs declines with reproductive aging, accompanied with more abnormal mitochondria. WHAT IS KNOWN ALREADY: Mitochondria play an important role in the dialogue between the mGCs and oocytes. However, the underlying mechanism of mitochondrial dysfunction in mGCs in aging is still poorly understood...
October 17, 2017: Human Reproduction
https://www.readbyqxmd.com/read/29040870/parkin-absence-accelerates-microtubule-aging-in-dopaminergic-neurons
#4
Daniele Cartelli, Alida Amadeo, Alessandra Maria Calogero, Francesca Vittoria Marialuisa Casagrande, Carmelita De Gregorio, Mariarosa Gioria, Naoko Kuzumaki, Ilaria Costa, Jenny Sassone, Andrea Ciammola, Nobutaka Hattori, Hideyuki Okano, Stefano Goldwurm, Laurent Roybon, Gianni Pezzoli, Graziella Cappelletti
Loss-of-function caused by mutations in the parkin gene (PARK2) lead to early-onset familial Parkinson's disease. Recently, mechanistic studies proved the ability of parkin in regulating mitochondria homeostasis and microtubule (MT) stability. Looking at these systems during aging of PARK2 knockout mice, we found that loss of parkin induced an accelerated (over)acetylation of MT system both in dopaminergic neuron cell bodies and fibers, localized in the substantia nigra and corpus striatum, respectively. Interestingly, in PARK2 knockout mice, changes of MT stability preceded the alteration of mitochondria transport...
September 20, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/29038583/zdhhc13-dependent-drp1-s-palmitoylation-impacts-brain-bioenergetics-anxiety-coordination-and-motor-skills
#5
Eleonora Napoli, Gyu Song, Siming Liu, Alexsandra Espejo, Carlos J Perez, Fernando Benavides, Cecilia Giulivi
Protein S-palmitoylation is a reversible post-translational modification mediated by palmitoyl acyltransferase enzymes, a group of Zn(2+)-finger DHHC-domain-containing proteins (ZDHHC). Here, for the first time, we show that Zdhhc13 plays a key role in anxiety-related behaviors and motor function, as well as brain bioenergetics, in a mouse model (luc) carrying a spontaneous Zdhhc13 recessive mutation. At 3 m of age, mutant mice displayed increased sensorimotor gating, anxiety, hypoactivity, and decreased motor coordination, compared to littermate controls...
October 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29038504/the-contribution-of-saccharomyces-cerevisiae-replicative-age-to-the-variations-in-the-levels-of-trx2p-pdr5p-can1p-and-idh-isoforms
#6
Aglaia V Azbarova, Kseniia V Galkina, Maxim I Sorokin, Fedor F Severin, Dmitry A Knorre
Asymmetrical division can be a reason for microbial populations heterogeneity. In particular, budding yeast daughter cells are more vulnerable to stresses than the mothers. It was suggested that yeast mother cells could also differ from each other depending on their replicative age. To test this, we measured the levels of Idh1-GFP, Idh2-GFP, Trx2-GFP, Pdr5-GFP and Can1-GFP proteins in cells of the few first, most represented, age cohorts. Pdr5p and Can1p were selected because of the pronounced mother-bud asymmetry for these proteins distributions, Trx2p as indicator of oxidative stress...
October 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29032504/resistance-exercise-improves-cardiac-function-and-mitochondrial-efficiency-in-diabetic-rat-hearts
#7
Tae Hee Ko, Jubert C Marquez, Hyoung Kyu Kim, Seung Hun Jeong, SungRyul Lee, Jae Boum Youm, In Sung Song, Dae Yun Seo, Hye Jin Kim, Du Nam Won, Kyoung Im Cho, Mun Gi Choi, Byoung Doo Rhee, Kyung Soo Ko, Nari Kim, Jong Chul Won, Jin Han
Metabolic disturbance and mitochondrial dysfunction are a hallmark of diabetic cardiomyopathy (DC). Resistance exercise (RE) not only enhances the condition of healthy individuals but could also improve the status of those with disease. However, the beneficial effects of RE in the prevention of DC and mitochondrial dysfunction are uncertain. Therefore, this study investigated whether RE attenuates DC by improving mitochondrial function using an in vivo rat model of diabetes. Fourteen Otsuka Long-Evans Tokushima Fatty rats were assigned to sedentary control (SC, n = 7) and RE (n = 7) groups at 28 weeks of age...
October 14, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/29030688/neurotrophic-function-of-phytochemicals-for-neuroprotection-in-aging-and-neurodegenerative-disorders-modulation-of-intracellular-signaling-and-gene-expression
#8
REVIEW
Makoto Naoi, Keiko Inaba-Hasegawa, Masayo Shamoto-Nagai, Wakako Maruyama
Bioactive compounds in food and beverages have been reported to promote health and prevent age-associated decline in cognitive, motor and sensory activities, and emotional function. Phytochemicals, a ubiquitous class of plant secondary metabolites, protect neuronal cells by interaction with cellular activities, in addition to the antioxidant and anti-inflammatory function. In aging and age-associated neurodegenerative disorders, phytochemicals protect neuronal cells by neurotrophic factor-mimic activity, in addition to suppression of apoptosis signaling in mitochondria...
October 13, 2017: Journal of Neural Transmission
https://www.readbyqxmd.com/read/29030433/dysregulation-of-the-mitochondrial-unfolded-protein-response-induces-non-apoptotic-dopaminergic-neurodegeneration-in-c-elegans-models-of-parkinson-s-disease
#9
Bryan A Martinez, Daniel A Petersen, Anthony L Gaeta, Samuel P Stanley, Guy A Caldwell, Kim A Caldwell
Due to environmental insult or innate genetic deficiency, protein folding environments of the mitochondrial matrix are prone to dysregulation, prompting the activation of a specific organellar stress-response mechanism the mitochondrial unfolded protein response (UPR(MT)). In Caenorhabditis elegans, mitochondrial damage leads to nuclear translocation of the ATFS-1 transcription factor to activate the UPR(MT) After short-term acute stress has been mitigated, the UPR(MT) is eventually suppressed to restore homeostasis to C...
October 13, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29029131/plasma-amino-acids-stimulate-uncoupled-respiration-of-muscle-subsarcolemmal-mitochondria-in-lean-but-not-obese-humans
#10
Katon A Kras, Nyssa Hoffman, Lori R Roust, Shivam H Patel, Chad C Carroll, Christos S Katsanos
Context: Obesity is associated with mitochondrial dysfunction in skeletal muscle. Increasing the plasma amino acid (AA) concentrations stimulates mitochondrial ATP production in lean individuals. Objective: To determine whether acute elevation in plasma AAs enhances muscle mitochondrial respiration and ATP production in subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria in obese adults. Design: Assessment of SS and IMF mitochondria function during saline (i...
September 28, 2017: Journal of Clinical Endocrinology and Metabolism
https://www.readbyqxmd.com/read/29025019/differing-molecular-response-of-young-and-advanced-maternal-age-human-oocytes-to-ivm
#11
J M Reyes, E Silva, J L Chitwood, W B Schoolcraft, R L Krisher, P J Ross
STUDY QUESTION: What effect does maternal age have on the human oocyte's molecular response to in vitro oocyte maturation? SUMMARY ANSWER: Although polyadenylated transcript abundance is similar between young and advanced maternal age (AMA) germinal vesicle (GV) oocytes, metaphase II (MII) oocytes exhibit a divergent transcriptome resulting from a differential response to in vitro oocyte maturation. WHAT IS KNOWN ALREADY: Microarray studies considering maternal age or maturation stage have shown that either of these factors will affect oocyte polyadenylated transcript abundance in human oocytes...
September 15, 2017: Human Reproduction
https://www.readbyqxmd.com/read/28994715/%C3%AE-amyloid-and-the-pathomechanisms-of-alzheimer-s-disease-a-comprehensive-view
#12
REVIEW
Botond Penke, Ferenc Bogár, Lívia Fülöp
Protein dyshomeostasis is the common mechanism of neurodegenerative diseases such as Alzheimer's disease (AD). Aging is the key risk factor, as the capacity of the proteostasis network declines during aging. Different cellular stress conditions result in the up-regulation of the neurotrophic, neuroprotective amyloid precursor protein (APP). Enzymatic processing of APP may result in formation of toxic Aβ aggregates (β-amyloids). Protein folding is the basis of life and death. Intracellular Aβ affects the function of subcellular organelles by disturbing the endoplasmic reticulum-mitochondria cross-talk and causing severe Ca(2+)-dysregulation and lipid dyshomeostasis...
October 10, 2017: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/28990533/blood-brain-barrier-disruption-leads-to-postoperative-cognitive-dysfunction
#13
Bin Wang, Siyuan Li, Xipeng Cao, Xinghui Dou, Jingzhu Li, Ling Wang, Mingshan Wang, Yanlin Bi
BACKGROUND: Postoperative cognitive dysfunction (POCD) has received considerable attention as one of the main postoperative complications. The underlying mechanism of POCD in elderly subjects has not been fully elucidated to date. The central nervous system (CNS) is isolated from the bloodstream by the blood brain barrier (BBB) that consists of endothelial cells, capillary blood vessels and the tight junctions. The tight junctions carry out significant biological functions that are associated with the CNS and the blood circulation...
October 9, 2017: Current Neurovascular Research
https://www.readbyqxmd.com/read/28987319/mitochondria-telomeres-and-cell-senescence-implications-for-lung-ageing-and-disease
#14
REVIEW
Jodie Birch, Peter J Barnes, Joao F Passos
Cellular senescence, the irreversible loss of replicative capacity in somatic cells, plays a causal role in the development of age-related pathology and in a number of age-related chronic inflammatory diseases. The ageing lung is marked by an increasing number of senescent cells, and evidence is mounting that senescence may directly contribute to a number of age-related respiratory diseases, including chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). Telomere dysfunction and alterations in mitochondrial homeostasis frequently occur in cellular senescence and are important to the development of the often detrimental senescence-associated secretory phenotype (SASP)...
October 4, 2017: Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/28986697/targeting-mitochondrial-function-and-proteostasis-to-mitigate-dynapenia
#15
REVIEW
Robert V Musci, Karyn L Hamilton, Benjamin F Miller
Traditionally, interventions to treat skeletal muscle aging have largely targeted sarcopenia-the age-related loss of skeletal muscle mass. Dynapenia refers to the age-related loss in skeletal muscle function due to factors outside of muscle mass, which helps to inform treatment strategies for aging skeletal muscle. There is evidence that mechanisms to maintain protein homeostasis and proteostasis, deteriorate with age. One key mechanism to maintain proteostasis is protein turnover, which is an energetically costly process...
October 6, 2017: European Journal of Applied Physiology
https://www.readbyqxmd.com/read/28986235/alpha-synuclein-epigenetics-mitochondria-metabolism-calcium-traffic-circadian-dysfunction-in-parkinson-s-disease-an-integrated-strategy-for-management
#16
REVIEW
Oliver T Phillipson
The motor deficits which characterise the sporadic form of Parkinson's disease arise from age-related loss of a subset of dopamine neurons in the substantia nigra. Although motor symptoms respond to dopamine replacement therapies, the underlying disease process remains. This review details some features of the progressive molecular pathology and proposes deployment of a combination of nutrients: R-lipoic acid, acetyl-l-carnitine, ubiquinol, melatonin (or receptor agonists) and vitamin D3, with the collective potential to slow progression of these features...
October 3, 2017: Ageing Research Reviews
https://www.readbyqxmd.com/read/28984759/serum-levels-of-uncoupling-proteins-in-patients-with-differential-insulin-resistance-a-community-based-cohort-study
#17
Heng-Chih Pan, Chin-Chan Lee, Kuei-Mei Chou, Shang-Chieh Lu, Chiao-Yin Sun
The uncoupling protein (UCP) belongs to a family of energy-dissipating proteins in mitochondria. Increasing evidences have indicated that UCPs have immense impact on glucose homeostasis and are key proteins in metabolic syndrome. For applying the findings to clinical practice, we designed a study to explore the association between serum UCPs 1-3 and insulin resistance. This investigation prospectively recorded demographical parameter and collected blood samples of 1071 participants from 4 districts in Northeastern Taiwan during the period from August 2013 to July 2014...
October 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/28984064/loss-of-sirt2-leads-to-axonal-degeneration-and-locomotor-disability-associated-with-redox-and-energy-imbalance
#18
Stéphane Fourcade, Laia Morató, Janani Parameswaran, Montserrat Ruiz, Tatiana Ruiz-Cortés, Mariona Jové, Alba Naudí, Paloma Martínez-Redondo, Mara Dierssen, Isidre Ferrer, Francesc Villarroya, Reinald Pamplona, Alejandro Vaquero, Manel Portero-Otín, Aurora Pujol
Sirtuin 2 (SIRT2) is a member of a family of NAD(+) -dependent histone deacetylases (HDAC) that play diverse roles in cellular metabolism and especially for aging process. SIRT2 is located in the nucleus, cytoplasm, and mitochondria, is highly expressed in the central nervous system (CNS), and has been reported to regulate a variety of processes including oxidative stress, genome integrity, and myelination. However, little is known about the role of SIRT2 in the nervous system specifically during aging. Here, we show that middle-aged, 13-month-old mice lacking SIRT2 exhibit locomotor dysfunction due to axonal degeneration, which was not present in young SIRT2 mice...
October 5, 2017: Aging Cell
https://www.readbyqxmd.com/read/28978719/pharmacological-dual-inhibition-of-tumor-and-tumor-induced-functional-limitations-in-transgenic-model-of-breast-cancer
#19
Ruizhong Wang, Poornima Bhat-Nakshatri, Maria B Padua, Mayuri S Prasad, Manjushree Anjanappa, Max Jacobson, Courtney Finnearty, Victoria Sefcsik, Kyle McElyea, Rachael Redmond, George E Sandusky, Narsimha Penthala, Peter A Crooks, Jianguo Liu, Teresa Zimmers, Harikrishna Nakshatri
Breast cancer progression is associated with systemic effects including functional limitations and sarcopenia without the appearance of overt cachexia. Autocrine/paracrine actions of cytokines/chemokines produced by cancer cells mediate cancer progression and functional limitations. The cytokine-inducible transcription factor NF-κB could be central to this process, as it displays oncogenic functions and is integral to the Pax7:MyoD:Pgc-1β:miR-486 myogenesis axis. We tested this possibility using the MMTV-PyMT transgenic mammary tumor model and the NF-κB inhibitor dimethylaminoparthenolide (DMAPT)...
October 4, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28975370/mesenchymal-stem-cells-from-preterm-to-term-newborns-undergo-a-significant-switch-from-anaerobic-glycolysis-to-the-oxidative-phosphorylation
#20
Silvia Ravera, Marina Podestà, Federica Sabatini, Chiara Fresia, Marta Columbaro, Silvia Bruno, Ezio Fulcheri, Luca Antonio Ramenghi, Francesco Frassoni
We evaluated the energy metabolism of human mesenchymal stem cells (MSC) isolated from umbilical cord (UC) of preterm (< 37 weeks of gestational age) and term (≥ 37 weeks of gestational age) newborns, using MSC from adult bone marrow as control. A metabolic switch has been observed around the 34th week of gestational age from a prevalently anaerobic glycolysis to the oxidative phosphorylation. This metabolic change is associated with the organization of mitochondria reticulum: preterm MSCs presented a scarcely organized mitochondrial reticulum and low expression of proteins involved in the mitochondrial fission/fusion, compared to term MSCs...
October 3, 2017: Cellular and Molecular Life Sciences: CMLS
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