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Mitochondria AND aging

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https://www.readbyqxmd.com/read/28446709/control-of-mitochondrial-biogenesis-and-function-by-the-ubiquitin-proteasome-system
#1
REVIEW
Piotr Bragoszewski, Michal Turek, Agnieszka Chacinska
Mitochondria are pivotal organelles in eukaryotic cells. The complex proteome of mitochondria comprises proteins that are encoded by nuclear and mitochondrial genomes. The biogenesis of mitochondrial proteins requires their transport in an unfolded state with a high risk of misfolding. The mislocalization of mitochondrial proteins is deleterious to the cell. The electron transport chain in mitochondria is a source of reactive oxygen species that damage proteins. Mitochondrial dysfunction is linked to many pathological conditions and, together with the loss of cellular protein homeostasis (proteostasis), are hallmarks of ageing and ageing-related degeneration diseases...
April 2017: Open Biology
https://www.readbyqxmd.com/read/28442351/major-depressive-disorder-mediates-accelerated-aging-in-rats-subjected-to-chronic-mild-stress
#2
Xiaoxian Xie, Yangyang Chen, Lingyan Ma, Qichen Shen, Liangfeng Huang, Binggong Zhao, Tao Wu, Zhengwei Fu
Major depressive disorder (MDD) has a complex etiology and is characterized by a change in mood and psychophysiological state. MDD has been shown to mediate accelerated biological aging in patients, although the underlying mechanism is not well understood. In the present study, we used a chronic mild stress (CMS) paradigm to induce anhedonia, one of the main symptoms of MDD. CMS induced depression-like symptoms in rats, including reduced sucrose preference and increased immobility time in the forced swim test...
April 22, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28440192/mitochondrial-permeability-transition-pore-as-a-suitable-target-for-neuroprotective-agents-against-alzheimer-disease
#3
Elena F Shevtsova, Daria Vinogradova, Margarita E Neganova, Marco Avila-Rodriguez, George E Barreto, Sergey O Bachurin, Gjumrakch Aliev
A considerable amount of data suggests the age-related impairments of mitochondrial functions in the development of sporadic forms of neurodegenerative pathologies. These includes a decrease in the calcium retention capacity of mitochondria, which leads to the disturbance of the functional activity of neurons, and increased sensitivity of mitochondria towards the induction of the permeability transition. This in turn provoke the neuronal death enhancing the development of neurodegenerative processes. Inhibitors of mitochondrial permeability transition, which increases calcium retention capacity of mitochondria, are considered as promising neuroprotective drugs able not only to halt the neurodegenerative cascade, but also to increase the functional activity of neurons...
April 23, 2017: CNS & Neurological Disorders Drug Targets
https://www.readbyqxmd.com/read/28439972/mitochondrial-biogenesis-and-pgc-1%C3%AE-gene-expression-in-male-broilers-from-ascites-susceptible-and-resistant-lines
#4
N Khodambashi Emami, A Golian, M Danesh Mesgaran, N B Anthony, D D Rhoads
Ascites is a cardiovascular metabolic disease characterized by accumulation of fluid around the heart and in the abdominal cavity that eventually leads to death. This syndrome is the end-point result of a series of metabolic incidents that are generally caused by impaired oxygen availability. Mitochondria are the major sites of oxygen consumption, therefore major contributors to oxidative stress. Genetic, metabolic and dietary factors can influence variations in mitochondrial biogenesis (mitochondrial size, number and mass) that might have an effect on oxygen consumption and reactive oxygen species production...
April 25, 2017: Journal of Animal Physiology and Animal Nutrition
https://www.readbyqxmd.com/read/28433662/iron-and-thiol-redox-signaling-in-cancer-an-exquisite-balance-to-escape-ferroptosis
#5
REVIEW
Shinya Toyokuni, Fumiya Ito, Kyoko Yamashita, Yasumasa Okazaki, Shinya Akatsuka
Epidemiological data indicate a constant worldwide increase in cancer mortality, although the age of onset is increasing. Recent accumulation of genomic data on human cancer via next-generation sequencing confirmed that cancer is a disease of genome alteration. In many cancers, the Nrf2 transcription system is activated via mutations either in Nrf2 or Keap1 ubiquitin ligase, leading to persistent activation of the genes with antioxidative functions. Furthermore, deep sequencing of passenger mutations is clarifying responsible cancer causative agent(s) in each case, including aging, APOBEC activation, smoking and UV...
April 19, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28432755/mitochondria-and-ageing-role-in-heart-skeletal-muscle-and-adipose-tissue
#6
REVIEW
Kerstin Boengler, Maik Kosiol, Manuel Mayr, Rainer Schulz, Susanne Rohrbach
Age is the most important risk factor for most diseases. Mitochondria play a central role in bioenergetics and metabolism. In addition, several lines of evidence indicate the impact of mitochondria in lifespan determination and ageing. The best-known hypothesis to explain ageing is the free radical theory, which proposes that cells, organs, and organisms age because they accumulate reactive oxygen species (ROS) damage over time. Mitochondria play a central role as the principle source of intracellular ROS, which are mainly formed at the level of complex I and III of the respiratory chain...
April 21, 2017: Journal of Cachexia, Sarcopenia and Muscle
https://www.readbyqxmd.com/read/28431562/effects-of-the-common-polymorphism-in-the-human-aldehyde-dehydrogenase-2-aldh2-gene-on-the-lung
#7
Aoi Kuroda, Ahmed E Hegab, Gao Jingtao, Shuji Yamashita, Nobuyuki Hizawa, Tohru Sakamoto, Hideyasu Yamada, Satoshi Suzuki, Makoto Ishii, Ho Namkoong, Takanori Asakura, Mari Ozaki, Hiroyuki Yasuda, Junko Hamamoto, Shizuko Kagawa, Kenzo Soejima, Tomoko Betsuyaku
BACKGROUND: Aldehyde dehydrogenases (ALDHs) play a major role in detoxification of aldehydes. High expression of ALDHs is a marker for stem cells of many organs including the lungs. A common polymorphism in ALDH2 gene (ALDH2*2) results in inactivation of the enzyme and is associated with alcohol flushing syndrome and increased risk for cardiovascular and Alzheimer's diseases and some cancers. The effect of this ALDH2 polymorphism on the lung and its stem cells has not been thoroughly examined...
April 21, 2017: Respiratory Research
https://www.readbyqxmd.com/read/28426722/interactions-between-mitoneet-and-naf-1-in-cells
#8
Ola Karmi, Sarah H Holt, Luhua Song, Sagi Tamir, Yuting Luo, Fang Bai, Ammar Adenwalla, Merav Darash-Yahana, Yang-Sung Sohn, Patricia A Jennings, Rajeev K Azad, Jose' N Onuchic, Faruck Morcos, Rachel Nechushtai, Ron Mittler
The NEET proteins mitoNEET (mNT) and nutrient-deprivation autophagy factor-1 (NAF-1) are required for cancer cell proliferation and resistance to oxidative stress. NAF-1 and mNT are also implicated in a number of other human pathologies including diabetes, neurodegeneration and cardiovascular disease, as well as in development, differentiation and aging. Previous studies suggested that mNT and NAF-1 could function in the same pathway in mammalian cells, preventing the over-accumulation of iron and reactive oxygen species (ROS) in mitochondria...
2017: PloS One
https://www.readbyqxmd.com/read/28424579/grp78-at-the-centre-of-the-stage-in-cancer-and-neuroprotection
#9
REVIEW
Caty Casas
The 78-kDa glucose-regulated protein GRP78, also known as BiP and HSP5a, is a multifunctional protein with activities far beyond its well-known role in the unfolded protein response (UPR) which is activated after endoplasmic reticulum (ER) stress in the cells. Most of these newly discovered activities depend on its position within the cell. GRP78 is located mainly in the ER, but it has also been observed in the cytoplasm, the mitochondria, the nucleus, the plasma membrane, and secreted, although it is dedicated mostly to engage endogenous cytoprotective processes...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28420950/metallothionein-copper-and-alpha-synuclein-in-alpha-synucleinopathies
#10
REVIEW
Yuho Okita, Alexandre N Rcom-H'cheo-Gauthier, Michael Goulding, Roger S Chung, Peter Faller, Dean L Pountney
Metallothioneins (MTs) are proteins that function by metal exchange to regulate the bioavailability of metals, such as zinc and copper. Copper functions in the brain to regulate mitochondria, neurotransmitter production, and cell signaling. Inappropriate copper binding can result in loss of protein function and Cu(I)/(II) redox cycling can generate reactive oxygen species. Copper accumulates in the brain with aging and has been shown to bind alpha-synuclein and initiate its aggregation, the primary aetiological factor in Parkinson's disease (PD), and other alpha-synucleinopathies...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28418993/solid-papillary-breast-carcinomas-resembling-the-tall-cell-variant-of-papillary-thyroid-neoplasms-a-unique-invasive-tumor-with-indolent-behavior
#11
Maria P Foschini, Sofia Asioli, Susan Foreid, Gabor Cserni, Ian O Ellis, Vincenzo Eusebi, Juan Rosai
Thirteen cases of invasive solid papillary breast carcinomas resembling the tall cell variant of papillary thyroid neoplasms (BPTC) are reported here. Some cases had long-term follow-up. BPTC is a special type of primary breast neoplasm showing a triple-negative profile but low aggressive potential. Knowledge on BPTC is still scanty; therefore, the aim of the present paper was to report on the features of an additional 13 cases. All the patients were female individuals, and the mean age at presentation was 62...
April 17, 2017: American Journal of Surgical Pathology
https://www.readbyqxmd.com/read/28413833/beneficial-effects-of-a-pyrroloquinolinequinone-containing-dietary-formulation-on-motor-deficiency-cognitive-decline-and-mitochondrial-dysfunction-in-a-mouse-model-of-alzheimer-s-disease
#12
Darrell Sawmiller, Song Li, Takashi Mori, Ahsan Habib, David Rongo, Vedad Delic, Patrick C Bradshaw, R Douglas Shytle, Cyndy Sanberg, Paula Bickford, Jun Tan
Alzheimer's disease (AD), a progressive neurodegenerative disorder, is linked to oxidative stress, altered amyloid precursor protein (APP) proteolysis, tau hyperphosphorylation and the accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFT). A growing body of evidence suggests that mitochondrial dysfunction can be a key promoter of all of these pathologies and predicts that restoration of mitochondrial function might be a potential therapeutic strategy for AD. Therefore, in the present study, we tested the beneficial effect of a nutraceutical formulation Nutrastem II (Nutra II), containing NT020 (a mitochondrial restorative and antioxidant proprietary formulation) and pyrroloquinolinequinone (PQQ, a stimulator of mitochondria biogenesis) in 5XFAD transgenic mice...
April 2017: Heliyon
https://www.readbyqxmd.com/read/28410198/specific-changes-in-mitochondrial-lipidome-alter-mitochondrial-proteome-and-increase-the-geroprotective-efficiency-of-lithocholic-acid-in-chronologically-aging-yeast
#13
Anna Leonov, Anthony Arlia-Ciommo, Simon D Bourque, Olivia Koupaki, Pavlo Kyryakov, Paméla Dakik, Mélissa McAuley, Younes Medkour, Karamat Mohammad, Tamara Di Maulo, Vladimir I Titorenko
We have previously found that exogenously added lithocholic acid delays yeast chronological aging. We demonstrated that lithocholic acid enters the yeast cell, is sorted to mitochondria, resides in both mitochondrial membranes, changes the relative concentrations of different membrane phospholipids, triggers changes in the concentrations of many mitochondrial proteins, and alters some key aspects of mitochondrial functionality. We hypothesized that the lithocholic acid-driven changes in mitochondrial lipidome may have a causal role in the remodeling of mitochondrial proteome, which may in turn alter the functional state of mitochondria to create a mitochondrial pattern that delays yeast chronological aging...
March 31, 2017: Oncotarget
https://www.readbyqxmd.com/read/28409855/the-mobility-of-mitochondria-intercellular-trafficking-in-health-and-disease
#14
Michael V Berridge, Jiri Neuzil
The view that genes are constrained within somatic cells is challenged by in vitro evidence, and more recently by in vivo studies which demonstrate that mitochondria with their mitochondrial DNA (mtDNA) payload not only can, but do move between cells in tumour models and in mouse models of tissue damage. Using mouse tumour cell models without mtDNA to reflect mtDNA damage, we have shown that these cells grow tumours only after acquiring mtDNA from cells in the local microenvironment resulting in respiration recovery, tumorigenesis and metastasis...
April 13, 2017: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/28407867/the-relationship-between-mitochondrial-dna-copy-number-and-stallion-sperm-function
#15
Christa R Darr, Luis E Moraes, Richard E Connon, Charles C Love, Sheila Teague, Dickson D Varner, Stuart A Meyers
Mitochondrial DNA (mtDNA) copy number has been utilized as a measure of sperm quality in several species including mice, dogs, and humans, and has been suggested as a potential biomarker of fertility in stallion sperm. The results of the present study extend this recent discovery using sperm samples from American Quarter Horse stallions of varying age. By determining copy number of three mitochondrial genes, cytochrome b (CYTB), NADH dehydrogenase 1 (ND1) and NADH dehydrogenase 4 (ND4), instead of a single gene, we demonstrate an improved understanding of mtDNA fate in stallion sperm mitochondria following spermatogenesis...
May 2017: Theriogenology
https://www.readbyqxmd.com/read/28407698/spermidine-coupled-with-exercise-rescues-skeletal-muscle-atrophy-from-d-gal-induced-aging-rats-through-enhanced-autophagy-and-reduced-apoptosis-via-ampk-foxo3a-signal-pathway
#16
Jingjing Fan, Xiaoqi Yang, Jie Li, Ziyang Shu, Jun Dai, Xingran Liu, Biao Li, Shaohui Jia, Xianjuan Kou, Yi Yang, Ning Chen
The quality control of skeletal muscle is a continuous requirement throughout the lifetime, although its functions and quality present as a declining trend during aging process. Dysfunctional or deficient autophagy and excessive apoptosis may contribute to the atrophy of senescent skeletal muscle. Spermidine, as a natural polyamine, can be involved in important cellular functions for lifespan extension and stress resistance in several model organisms through activating autophagy. Similarly, cellular autophagic responses to exercise have also been extensively investigated...
March 14, 2017: Oncotarget
https://www.readbyqxmd.com/read/28405769/study-on-the-apoptosis-mediated-by-cytochrome-c-and-factors-that-affect-the-activation-of-bovine-longissimus-muscle-during-postmortem-aging
#17
Jiaying Zhang, Qunli Yu, Ling Han, Cheng Chen, Hang Li, Guangxing Han
This study investigates whether bovine longissimus muscle cell apoptosis occurs during postmortem aging and whether apoptosis is dependent on the mitochondria pathway. This study also determines the apoptosis process mediated by cytochrome c after its release from mitochondria and the factors that affect the activation processes. Results indicate that apoptotic nuclei were detected at 12 h postmortem. Cytochrome c release from the mitochondria to the cytoplasm activated the caspase-9 and caspase-3 at early postmortem aging and the activation of caspase-9 occurs before the activation of caspase-3...
June 2017: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/28400824/melatonin-and-human-mitochondrial-diseases
#18
REVIEW
Reza Sharafati-Chaleshtori, Hedayatollah Shirzad, Mahmoud Rafieian-Kopaei, Amin Soltani
Mitochondrial dysfunction is one of the main causative factors in a wide variety of complications such as neurodegenerative disorders, ischemia/reperfusion, aging process, and septic shock. Decrease in respiratory complex activity, increase in free radical production, increase in mitochondrial synthase activity, increase in nitric oxide production, and impair in electron transport system and/or mitochondrial permeability are considered as the main factors responsible for mitochondrial dysfunction. Melatonin, the pineal gland hormone, is selectively taken up by mitochondria and acts as a powerful antioxidant, regulating the mitochondrial bioenergetic function...
2017: Journal of Research in Medical Sciences: the Official Journal of Isfahan University of Medical Sciences
https://www.readbyqxmd.com/read/28398002/alpha-ketoglutarate-curbs-differentiation-and-induces-cell-death-in-mesenchymal-stromal-precursors-with-mitochondrial-dysfunction
#19
Karmveer Singh, Linda Krug, Abhijit Basu, Patrick Meyer, Nicolai Treiber, Seppe Vander Beken, Meinhard Wlaschek, Stefan Kochanek, Wilhelm Bloch, Hartmut Geiger, Pallab Maity, Karin Scharffetter-Kochanek
Increased concentrations of reactive oxygen species (ROS) originating from dysfunctional mitochondria contribute to diverse aging-related degenerative disorders. But so far little is known about the impact of distinct ROS on metabolism and fate of stromal precursor cells. We here demonstrate that an increase in superoxide anion radicals due to superoxide dismutase 2 (Sod2) deficiency in stromal precursor cells suppress osteogenic and adipogenic differentiation through fundamental changes in the global metabolite landscape...
April 11, 2017: Stem Cells
https://www.readbyqxmd.com/read/28397282/brain-aging-and-neurodegeneration-from-a-mitochondrial-point-of-view
#20
REVIEW
Amandine Grimm, Anne Eckert
Aging was defined as a progressive time-related accumulation of changes responsible for or at least involved in the increased susceptibility to disease and death. The brain seems to be particularly sensitive to the aging process since the appearance of neurodegenerative diseases, including Alzheimer's disease, is exponential with the increasing age. Mitochondria were placed at the center of the "free-radical theory of aging", because these paramount organelles are not only the main producers of energy in the cells, but also to main source of reactive oxygen species (ROS)...
April 11, 2017: Journal of Neurochemistry
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