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Mitochondria AND aging

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https://www.readbyqxmd.com/read/28822845/triphenyl-phosphonium-coated-nano-quercetin-for-oral-delivery-neuroprotective-effects-in-attenuating-age-related-global-moderate-cerebral-ischemia-reperfusion-injury-in-rats
#1
Swarupa Ghosh, Sibani Sarkar, Somsubhra T Choudhury, Tirtha Ghosh, Nirmalendu Das
Cerebral ischemia-reperfusion is a classical example of reactive oxygen species (ROS) mediated acute damage to brain. Post-ischemic reperfusion induced oxygen free radicals production causes damage to brain cell mitochondria. Antioxidants like quercetin (Qc) have potentials to manage oxidative stress related pathophysiology. However low oral bioavailability and poor cell membrane permeability restricts its therapeutic efficacy. To overcome these hurdles mitochondria specific delivery of Qc nanocapsules were designed to efficiently counteract cerebral ischemia-reperfusion induced cell death and neurodegeneration in young and aged rats...
August 16, 2017: Nanomedicine: Nanotechnology, Biology, and Medicine
https://www.readbyqxmd.com/read/28819942/study-of-the-relationship-between-ages-and-oxidative-stress-damage-to-trophoblast-cell-mitochondria
#2
Lingling Jiang, Jianying Yan, Lixiang Wu
OBJECTIVES: To study the influence of AGEs on placental trophoblast mitochondria oxidative stress, and to explore the possible pathogenesis which may participate in pre-eclampsia. MATERIAL AND METHODS: Human trophoblast cells from early pregnancy were cultured by an enzyme-digestion method. When trophoblast cells reached approximately 70-80% after passages, they were incubated with pre-eclampsia serum for 24 hours. A fluorescent dye assay was applied to measure the mitochondrial membrane potential; ELISA was used to measure the activity of the mitochondrial permeability transition pore...
2017: Ginekologia Polska
https://www.readbyqxmd.com/read/28818596/cardiometabolic-phenotypes-and-mitochondrial-dna-copy-number-in-two-cohorts-of-uk-women
#3
Anna L Guyatt, Kimberley Burrows, Philip A I Guthrie, Sue Ring, Wendy McArdle, Ian N M Day, Raimondo Ascione, Debbie A Lawlor, Tom R Gaunt, Santiago Rodriguez
The mitochondrial genome is present at variable copy number between individuals. Mitochondria are vulnerable to oxidative stress, and their dysfunction may be associated with cardiovascular disease. The association of mitochondrial DNA copy number with cardiometabolic risk factors (lipids, glycaemic traits, inflammatory markers, anthropometry and blood pressure) was assessed in two independent cohorts of European origin women, one in whom outcomes were measured at mean (SD) age 30 (4.3) years (N=2278) and the second at 69...
August 14, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28815529/mitochondrial-associated-membranes-in-parkinson-s-disease
#4
Nobutaka Hattori, Taku Arano, Taku Hatano, Akio Mori, Yuzuru Imai
Parkinson's disease (PD) is a common neurodegenerative disorder, with ageing being a major risk factor. Accordingly, estimates predict an increasing number of PD patients due to our expanding life span. Consequently, developing a true disease-modifying therapy is necessary. In this regard, monogenic PD offers a suitable means for determining pathogenesis. Among monogenic forms of PD, mitochondrial dysfunction may be a major cause and is also likely to be involved in sporadic PD. Thus, mitochondrial impairment may be a common pathway...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28814984/protective-mechanisms-of-the-mitochondrial-derived-peptide-humanin-in-oxidative-and-endoplasmic-reticulum-stress-in-rpe-cells
#5
REVIEW
Leonid Minasyan, Parameswaran G Sreekumar, David R Hinton, Ram Kannan
Age-related macular degeneration (AMD) is the leading cause of severe and irreversible vision loss and is characterized by progressive degeneration of the retina resulting in loss of central vision. The retinal pigment epithelium (RPE) is a critical site of pathology of AMD. Mitochondria and the endoplasmic reticulum which lie in close anatomic proximity to each other are targets of oxidative stress and endoplasmic reticulum (ER) stress, respectively, and contribute to the progression of AMD. The two organelles exhibit close interactive function via various signaling mechanisms...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28811869/pro-and-antioxidant-functions-of-the-peroxisome-mitochondria-connection-and-its-impact-on-aging-and-disease
#6
REVIEW
Amparo Pascual-Ahuir, Sara Manzanares-Estreder, Markus Proft
Peroxisomes and mitochondria are the main intracellular sources for reactive oxygen species. At the same time, both organelles are critical for the maintenance of a healthy redox balance in the cell. Consequently, failure in the function of both organelles is causally linked to oxidative stress and accelerated aging. However, it has become clear that peroxisomes and mitochondria are much more intimately connected both physiologically and structurally. Both organelles share common fission components to dynamically respond to environmental cues, and the autophagic turnover of both peroxisomes and mitochondria is decisive for cellular homeostasis...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28809938/perinatal-testosterone-exposure-potentiates-vascular-dysfunction-by-er%C3%AE-suppression-in-endothelial-progenitor-cells
#7
Weiguo Xie, Mingming Ren, Ling Li, Yin Zhu, Zhigang Chu, Zhigang Zhu, Qiongfang Ruan, Wenting Lou, Haimou Zhang, Zhen Han, Xiaodong Huang, Wei Xiang, Tao Wang, Paul Yao
Recent clinical cohort study shows that testosterone therapy increases cardiovascular diseases in men with low testosterone levels, excessive circulating androgen levels may play a detrimental role in the vascular system, while the potential mechanism and effect of testosterone exposure on the vascular function in offspring is still unknown. Our preliminary results showed that perinatal testosterone exposure in mice induces estrogen receptor β (ERβ) suppression in endothelial progenitor cells (EPCs) in offspring but not mothers, while estradiol (E2) had no effect...
2017: PloS One
https://www.readbyqxmd.com/read/28808064/obesity-and-aging-diminish-sirt1-mediated-deacetylation-of-sirt3-leading-to-hyperacetylation-and-decreased-activity-and-stability-of-sirt3
#8
Sanghoon Kwon, Sunmi Seok, Peter Yau, Xiaoling Li, Byron Kemper, Jongsook Kim Kemper
Sirtuin 3 (SIRT3) deacetylates and regulates many mitochondrial proteins to maintain health, but its functions are depressed in aging and obesity. The best-studied sirtuin, SIRT1, counteracts aging- and obesity-related diseases by deacetylating many proteins, but whether SIRT1 has a role in deacetylating and altering the function of SIRT3 is unknown. Here we show that SIRT3 is reversibly acetylated in the mitochondria and unexpectedly is a target of SIRT1 deacetylation. SIRT3 is hyperacetylated in aged and obese mice, in which SIRT1 activity is low, and SIRT3 acetylation at K57 inhibits its deacetylase activity and promotes protein degradation...
August 14, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28807550/decreased-gene-expression-of-fatty-acid-binding-protein-3-in-the-atrium-of-patients-with-new-onset-of-atrial-fibrillation-in-cardiac-perioperative-phase
#9
Yasushige Shingu, Takashi Yokota, Shingo Takada, Haruki Niwano, Tomonori Ooka, Hiroki Katoh, Tsuyoshi Tachibana, Suguru Kubota, Yoshiro Matsui
BACKGROUND: Post-operative atrial fibrillation (POAF) frequently occurs after cardiac surgery. However, the mechanisms of POAF have not been fully elucidated. We aimed to examine whether pre-operative atrial gene expression related to cardiac metabolism is changed in patients with POAF. METHODS: Right atrial tissue was obtained during surgery from 38 patients who underwent cardiac surgery from 2013 to 2015. Atrial expression levels were determined by reverse transcription polymerase chain reaction for the following genes: glucose transporter type 4, peroxisome proliferator-activated receptor-α, fatty acid translocase, carnitine palmitoyltransferase 1B, and fatty acid binding protein 3 (FABP3)...
August 11, 2017: Journal of Cardiology
https://www.readbyqxmd.com/read/28804760/autopsy-case-of-the-c12orf65-mutation-in-a-patient-with-signs-of-mitochondrial-dysfunction
#10
Hideaki Nishihara, Masatoshi Omoto, Masaki Takao, Yujiro Higuchi, Michiaki Koga, Motoharu Kawai, Hiroo Kawano, Eiji Ikeda, Hiroshi Takashima, Takashi Kanda
OBJECTIVE: To describe the autopsy case of a patient with a homozygous 2-base deletion, c171_172delGA (p.N58fs), in the C12orf65 gene. METHODS: We described the clinical history, neuroimaging data, neuropathology, and genetic analysis of the patients with C12orf65 mutations. RESULTS: The patient was a Japanese woman with a history of delayed psychomotor development, primary amenorrhea, and gait disturbance in her 20s. She was hospitalized because of respiratory failure at the age of 60...
August 2017: Neurology. Genetics
https://www.readbyqxmd.com/read/28799020/from-discovery-of-the-chop-axis-and-targeting-clpp-to-the-identification-of-additional-axes-of-the-uprmt-driven-by-the-estrogen-receptor-and-sirt3
#11
Timothy C Kenny, Doris Germain
The mitochondrial UPR (UPR(mt)) is rapidly gaining attention. While most studies on the UPR(mt) have focused on its role in aging, emerging studies suggest an important role of the UPR(mt) in cancer. Further, several of the players of the UPR(mt) in mammalian cells have well reported roles in the maintenance of the organelle. The goal of this review is to emphasize aspects of the UPR(mt) that have been overlooked in the current literature, describe the role of specific players of the UPR(mt) in the biology of the mitochondria and highlight the intriguing possibility that targeting the UPR(mt) in cancer may be already within reach...
August 10, 2017: Journal of Bioenergetics and Biomembranes
https://www.readbyqxmd.com/read/28795394/mitophagy-in-maintaining-skeletal-muscle-mitochondrial-proteostasis-and-metabolic-health-with-aging
#12
Joshua C Drake, Zhen Yan
Skeletal muscle is important for overall functionality and health. Aging is associated with an accumulation of damage to mitochondria DNA and proteins. In particular, damage to mitochondrial proteins in skeletal muscle, which is a loss of mitochondrial proteostasis, contributes to tissue dysfunction and negatively impacts systemic health. Therefore, understanding the mechanisms underlying the regulation of mitochondrial proteostasis and how those mechanisms change with age is important for the development of interventions to promote healthy aging...
August 10, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28792006/mitochondrial-diseases-the-contribution-of-organelle-stress-responses-to-pathology
#13
REVIEW
Anu Suomalainen, Brendan J Battersby
Mitochondrial diseases affect one in 2,000 individuals; they can present at any age and they can manifest in any organ. How defects in mitochondria can cause such a diverse range of human diseases remains poorly understood. Insight into this diversity is emerging from recent research that investigated defects in mitochondrial protein synthesis and mitochondrial DNA maintenance, which showed that many cell-specific stress responses are induced in response to mitochondrial dysfunction. Studying the molecular regulation of these stress responses might increase our understanding of the pathogenesis and variability of human mitochondrial diseases...
August 9, 2017: Nature Reviews. Molecular Cell Biology
https://www.readbyqxmd.com/read/28791889/symbiotic-origin-of-aging
#14
Edward Greenberg, Sergei Vatolin
Normally aging cells are characterized by an unbalanced mitochondrial dynamic skewed toward punctate mitochondria. Genetic and pharmacological manipulation of mitochondrial fission/fusion cycles can contribute to both accelerated and decelerated cellular or organismal aging. In this work, we connect these experimental data with the symbiotic theory of mitochondrial origin to generate new insight into the evolutionary origin of aging. Mitochondria originated from autotrophic α-proteobacteria during an ancient endosymbiotic event early in eukaryote evolution...
August 9, 2017: Rejuvenation Research
https://www.readbyqxmd.com/read/28789970/mitochondrial-fusion-fission-and-mitochondrial-toxicity
#15
Joel N Meyer, Tess C Leuthner, Anthony L Luz
Mitochondrial dynamics are regulated by two sets of opposed processes: mitochondrial fusion and fission, and mitochondrial biogenesis and degradation (including mitophagy), as well as processes such as intracellular transport. These processes maintain mitochondrial homeostasis, regulate mitochondrial form, volume and function, and are increasingly understood to be critical components of the cellular stress response. Mitochondrial dynamics vary based on developmental stage and age, cell type, environmental factors, and genetic background...
August 5, 2017: Toxicology
https://www.readbyqxmd.com/read/28783712/machine-learning-for-predicting-lifespan-extending-chemical-compounds
#16
Diogo G Barardo, Danielle Newby, Daniel Thornton, Taravat Ghafourian, João Pedro de Magalhães, Alex A Freitas
Increasing age is a risk factor for many diseases; therefore developing pharmacological interventions that slow down ageing and consequently postpone the onset of many age-related diseases is highly desirable. In this work we analyse data from the DrugAge database, which contains chemical compounds and their effect on the lifespan of model organisms. Predictive models were built using the machine learning method random forests to predict whether or not a chemical compound will increase Caenorhabditis elegans' lifespan, using as features Gene Ontology (GO) terms annotated for proteins targeted by the compounds and chemical descriptors calculated from each compound's chemical structure...
July 18, 2017: Aging
https://www.readbyqxmd.com/read/28782874/in-vivo-imaging-reveals-mitophagy-independence-in-the-maintenance-of-axonal-mitochondria-during-normal-aging
#17
Xu Cao, Haiqiong Wang, Zhao Wang, Qingyao Wang, Shuang Zhang, Yuanping Deng, Yanshan Fang
Mitophagy is thought to be a critical mitochondrial quality control mechanism in neurons and has been extensively studied in neurological disorders such as Parkinson's disease. However, little is known about how mitochondria are maintained in the lengthy neuronal axons in the context of physiological aging. Here, we utilized the unique Drosophila wing nerve model and in vivo imaging to rigorously profile changes in axonal mitochondria during aging. We revealed that mitochondria became fragmented and accumulated in aged axons...
August 7, 2017: Aging Cell
https://www.readbyqxmd.com/read/28780002/sex-specific-gene-expression-and-life-span-regulation
#18
REVIEW
John Tower
Aging-related diseases show a marked sex bias. For example, women live longer than men yet have more Alzheimer's disease and osteoporosis, whereas men have more cancer and Parkinson's disease. Understanding the role of sex will be important in designing interventions and in understanding basic aging mechanisms. Aging also shows sex differences in model organisms. Dietary restriction (DR), reduced insulin/IGF1-like signaling (IIS), and reduced TOR signaling each increase life span preferentially in females in both flies and mice...
August 2, 2017: Trends in Endocrinology and Metabolism: TEM
https://www.readbyqxmd.com/read/28776263/age-and-ischemia-differentially-impact-mitochondrial-ultrastructure-and-function-in-a-novel-model-of-age-associated-estrogen-deficiency-in-the-female-rat-heart
#19
Alexandra M Garvin, Nicole C Aurigemma, Jenna L Hackenberger, Donna H Korzick
Altered mitochondrial respiration, morphology, and quality control collectively contribute to mitochondrial dysfunction in the aged heart. Because myocardial infarction remains the leading cause of death in aged women, the present study utilized a novel rodent model to recapitulate human menopause to interrogate the combination of age and estrogen deficiency on mitochondrial ultrastructure and function with cardiac ischemia/reperfusion (I/R) injury. Female F344 rats were ovariectomized (OVX) at 15 months and studied at 24 months (MO OVX; n = 40) vs adult ovary intact (6 months; n = 41)...
August 4, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28768533/progression-of-pathology-in-pink1-deficient-mouse-brain-from-splicing-via-ubiquitination-er-stress-and-mitophagy-changes-to-neuroinflammation
#20
Sylvia Torres-Odio, Jana Key, Hans-Hermann Hoepken, Júlia Canet-Pons, Lucie Valek, Bastian Roller, Michael Walter, Blas Morales-Gordo, David Meierhofer, Patrick N Harter, Michel Mittelbronn, Irmgard Tegeder, Suzana Gispert, Georg Auburger
BACKGROUND: PINK1 deficiency causes the autosomal recessive PARK6 variant of Parkinson's disease. PINK1 activates ubiquitin by phosphorylation and cooperates with the downstream ubiquitin ligase PARKIN, to exert quality control and control autophagic degradation of mitochondria and of misfolded proteins in all cell types. METHODS: Global transcriptome profiling of mouse brain and neuron cultures were assessed in protein-protein interaction diagrams and by pathway enrichment algorithms...
August 2, 2017: Journal of Neuroinflammation
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