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Mitochondria AND aging

Snehal N Chaudhari, Edward T Kipreos
Fused, elongated mitochondria are more efficient in generating ATP than fragmented mitochondria. In diverse C. elegans longevity pathways, increased levels of fused mitochondria are associated with lifespan extension. Blocking mitochondrial fusion in these animals abolishes their extended longevity. The long-lived C. elegans vhl-1 mutant is an exception that does not have increased fused mitochondria, and is not dependent on fusion for longevity. Loss of mammalian VHL upregulates alternate energy generating pathways...
June 14, 2018: BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology
Yexing Xian, Lifeng Liang, Shutao Qi, Yingjun Xie, Bing Song, Shuming Ouyang, Yuhuan Xie, Xiaofang Sun, Weihua Wang
The aim of the present study was to verify the effects of heavy metal coupling agents (sodium citrate and EDTA) and antioxidants (acetyl carnitine and lipoic acid) on the number of oocytes, as well as the ageing of mitochondria, chromosomes and spindles in mice. C57BL/6 female mice were randomly classified into four groups (n=12 per group): i) Heavy metal coupling agent; ii) antioxidant; iii) mixed group; and iv) the normal control group. For the treatments, heavy metal coupling agents and antioxidants were added to the drinking water provided to the mice...
June 14, 2018: Molecular Medicine Reports
Yoshio Ogura, Munehiro Kitada, Itaru Monno, Keizo Kanasaki, Ai Watanabe, Daisuke Koya
OBJECTIVES: Mitochondrial oxidative stress is involved in the pathogenesis of diabetic kidney disease. The objective of our study is to identify the mechanisms of renal mitochondrial oxidative stress, focusing on Sirt3, which is nicotinamide adenine dinucleotide (NAD+ ; oxidized NAD)-dependent deacetylase in mitochondria. METHODS: Renal mitochondrial oxidative stress and Sirt3 activity, using Zucker diabetic fatty rats (ZDFRs) and cultured proximal tubular cells under high-glucose condition were evaluated...
December 2018: Redox Report: Communications in Free Radical Research
Joshua C Drake
No abstract text is available yet for this article.
June 13, 2018: Journal of Physiology
Chinthasagar Bastian, Jane Zaleski, Katharine Stahon, Brandon Parr, Andrew McCray, Jerica Day, Sylvain Brunet, Selva Baltan
White matter (WM) damage following a stroke underlies a majority of the neurological disability that is subsequently observed. Although ischemic injury mechanisms are age-dependent, conserving axonal mitochondria provides consistent post-ischemic protection to young and aging WM. Nitric Oxide Synthase (NOS) activation is a major cause of oxidative and mitochondrial injury in gray matter during ischemia; therefore, we used a pure WM tract, isolated male mouse optic nerve, to investigate whether NOS inhibition provides post-ischemic functional recovery by preserving mitochondria...
June 11, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Yiyang Wang, Jieliang Shen, Yanyang Chen, Huzhe Liu, Hao Zhou, Zhibiao Bai, Zhenming Hu
Intervertebral disc degeneration (IDD) is closely related with aging, whereas mitochondrial dysfunction is a common feature of aging in which results cell senescence. Phosphatase and tensin homolog (PTEN)-induced putative kinase protein 1 (PINK1) is a mitochondrial-targeted serine/threonine kinase, which plays a protective role against mitochondrial dysfunction with mitochondrial quality control by activating PINK1/Parkin mediated mitophagy. This study aimed to investigate the protective role of PINK1 against mitochondrial dysfunction and human nucleus pulposus cell (NPC) senescence...
June 8, 2018: Biochemical and Biophysical Research Communications
Mathieu Panel, Bijan Ghaleh, Didier Morin
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. As the mitochondrion is an important source of reactive oxygen species (ROS), this organelle is regarded as a key intracellular player in this process and a large amount of data supports the role of mitochondrial ROS production during aging...
June 11, 2018: Aging Cell
Su-Jeong Kim, Hemal H Mehta, Junxiang Wan, Chisaka Kuehnemann, Jingcheng Chen, Ji-Fan Hu, Andrew R Hoffman, Pinchas Cohen
Cellular senescence is a complex cell fate response that is thought to underlie several age-related pathologies. Despite a loss of proliferative potential, senescent cells are metabolically active and produce energy-consuming effectors, including senescence-associated secretory phenotypes (SASPs). Mitochondria play crucial roles in energy production and cellular signaling, but the key features of mitochondrial physiology and particularly of mitochondria-derived peptides (MDPs), remain underexplored in senescence responses...
June 10, 2018: Aging
Dori C Woods, Konstantin Khrapko, Jonathan L Tilly
Contrasting the equal contribution of nuclear genetic material from maternal and paternal sources to offspring, passage of mitochondria, and thus mitochondrial DNA (mtDNA), is uniparental through the egg. Since mitochondria in eggs are ancestral to all somatic mitochondria of the next generation and to all cells of future generations, oocytes must prepare for the high energetic demands of maturation, fertilization and embryogenesis while simultaneously ensuring that their mitochondrial genomes are inherited in an undamaged state...
May 21, 2018: Genes
Irina Odinokova, Yulia Baburina, Alexey Kruglov, Irina Fadeeva, Alena Zvyagina, Linda Sotnikova, Vladimir Akatov, Olga Krestinina
Excessive generation of reactive oxygen species (ROS) in mitochondria and the opening of the nonselective mitochondrial permeability transition pore are important factors that promote cardiac pathologies and dysfunction. The hormone melatonin (MEL) is known to improve the functional state of mitochondria via an antioxidant effect. Here, the effect of MEL administration on heart mitochondria from aged rats with acute cardiac failure caused by isoprenaline hydrochloride (ISO) was studied. A histological analysis revealed that chronic intake of MEL diminished the age-dependent changes in the structure of muscle fibers of the left ventricle, muscle fiber swelling, and injury zones characteristic of acute cardiac failure caused by ISO...
May 23, 2018: International Journal of Molecular Sciences
M Kotula-Balak, P Pawlicki, A Milon, W Tworzydlo, M Sekula, A Pacwa, E Gorowska-Wojtowicz, B Bilinska, B Pawlicka, J Wiater, M Zarzycka, J Galas
In this study, G-coupled estrogen receptor (GPER) was inactivated, by treatment with antagonist (G-15), in testes of C57BL/6 mice: immature (3 weeks old), mature (3 months old) and aged (1.5 years old) (50 μg/kg bw), as well as MA-10 mouse Leydig cells (10 nM/24 h) alone or in combination with 17β-estradiol or antiestrogen (ICI 182,780). In G-15-treated mice, overgrowth of interstitial tissue was found in both mature and aged testes. Depending on age, differences in structure and distribution of various Leydig cell organelles were observed...
June 6, 2018: Cell and Tissue Research
Vinay Lanke, S T R Moolamalla, Dipanjan Roy, P K Vinod
Alzheimer's disease (AD) is a neurodegenerative disorder contributing to rapid decline in cognitive function and ultimately dementia. Most cases of AD occur in elderly and later years. There is a growing need for understanding the relationship between aging and AD to identify shared and unique hallmarks associated with the disease in a region and cell-type specific manner. Although genomic studies on AD have been performed extensively, the molecular mechanism of disease progression is still not clear. The major objective of our study is to obtain a higher-order network-level understanding of aging and AD, and their relationship using the hippocampal gene expression profiles of young (20-50 years), aging (70-99 years), and AD (70-99 years)...
2018: Frontiers in Aging Neuroscience
David C Schöndorf, Dina Ivanyuk, Pascale Baden, Alvaro Sanchez-Martinez, Silvia De Cicco, Cong Yu, Ivana Giunta, Lukas K Schwarz, Gabriele Di Napoli, Vasiliki Panagiotakopoulou, Sigrun Nestel, Marcus Keatinge, Jan Pruszak, Oliver Bandmann, Bernd Heimrich, Thomas Gasser, Alexander J Whitworth, Michela Deleidi
While mitochondrial dysfunction is emerging as key in Parkinson's disease (PD), a central question remains whether mitochondria are actual disease drivers and whether boosting mitochondrial biogenesis and function ameliorates pathology. We address these questions using patient-derived induced pluripotent stem cells and Drosophila models of GBA-related PD (GBA-PD), the most common PD genetic risk. Patient neurons display stress responses, mitochondrial demise, and changes in NAD+ metabolism. NAD+ precursors have been proposed to ameliorate age-related metabolic decline and disease...
June 5, 2018: Cell Reports
Amy K Reeve, John P Grady, Eve M Cosgrave, Emma Bennison, Chun Chen, Philippa D Hepplewhite, Christopher M Morris
Mitochondrial dysfunction within the cell bodies of substantia nigra neurons is prominent in both ageing and Parkinson's disease. The loss of dopaminergic substantia nigra neurons in Parkinson's disease is associated with loss of synapses within the striatum, and this may precede neuronal loss. We investigated whether mitochondrial changes previously reported within substantia nigra neurons were also seen within the synapses and axons of these neurons. Using high resolution quantitative fluorescence immunohistochemistry we determined mitochondrial density within remaining dopaminergic axons and synapses, and quantified deficiencies of mitochondrial Complex I and Complex IV in these compartments...
2018: NPJ Parkinson's Disease
Meytal Radzinski, Rosi Fassler, Ohad Yogev, William Breuer, Nadav Shai, Jenia Gutin, Sidra Ilyas, Yifat Geffen, Sabina Tsytkin-Kirschenzweig, Yaakov Nahmias, Tommer Ravid, Nir Friedman, Maya Shuldiner, Dana Reichmann
Cellular redox status affects diverse cellular functions, including proliferation, protein homeostasis, and aging. Thus, individual differences in redox status can give rise to distinct sub-populations even among cells with identical genetic backgrounds. Here, we have created a novel methodology to track redox status at single cell resolution using the redox-sensitive probe Grx1-roGFP2. Our method allows identification and sorting of sub-populations with different oxidation levels in either the cytosol, mitochondria or peroxisomes...
June 5, 2018: ELife
Y X Mao, W J Cai, X Y Sun, P P Dai, X M Li, Q Wang, X L Huang, B He, P P Wang, G Wu, J F Ma, S B Huang
Advanced glycation end products (AGEs) can stimulate osteoblast apoptosis and have a critical role in the pathophysiology of diabetic osteoporosis. Mitochondrial abnormalities are closely related to osteoblast dysfunction. However, it remains unclear whether mitochondrial abnormalities are involved in AGE-induced osteoblastic cell apoptosis. Silibinin, a major flavonolignan compound of silimarin, has strong antioxidant and mitochondria-protective properties. In the present study, we explored the possible mitochondrial mechanisms underlying AGE-induced apoptosis of osteoblastic cells and the effect of silibinin on osteoblastic cell apoptosis...
June 4, 2018: Cell Death & Disease
Siva S V P Sakamuri, Jared A Sperling, Venkata N Sure, Monica H Dholakia, Nicholas R Peterson, Ibolya Rutkai, Padmini S Mahalingam, Ryosuke Satou, Prasad V G Katakam
Mitochondria play a critical role in the cardiomyocyte physiology by generating majority of the ATP required for the contraction/relaxation through oxidative phosphorylation (OXPHOS). Aging is a major risk factor for cardiovascular diseases (CVD) and mitochondrial dysfunction has been proposed as potential cause of aging. Recent technological innovations in Seahorse XFe24 Analyzer enhanced the detection sensitivity of oxygen consumption rate and proton flux to advance our ability study mitochondrial function...
June 2, 2018: GeroScience
Susana Cadenas
Mitochondrial oxidative phosphorylation is incompletely coupled, since protons translocated to the intermembrane space by specific respiratory complexes of the electron transport chain can return to the mitochondrial matrix independently of the ATP synthase -a process known as proton leak- generating heat instead of ATP. Proton leak across the inner mitochondrial membrane increases the respiration rate and decreases the electrochemical proton gradient (Δp), and is an important mechanism for energy dissipation that accounts for up to 25% of the basal metabolic rate...
May 31, 2018: Biochimica et Biophysica Acta
Tianren Wang, Elnur Babayev, Zongliang Jiang, Guangxin Li, Man Zhang, Ecem Esencan, Tamas Horvath, Emre Seli
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. A 4-fold increase in atretic follicles at 3 months, and reduced number of primordial follicles at 6-12 months are observed in Clpp-/- ovaries...
May 30, 2018: Aging Cell
Jan Suski, Magdalena Lebiedzinska, Massimo Bonora, Paolo Pinton, Jerzy Duszynski, Mariusz R Wieckowski
Mitochondria are considered the main source of reactive oxygen species (ROS) in the cell. For this reason they have been recognized as a source of various pathological conditions as well as aging. Chronic increase in the rate of ROS production is responsible for the accumulation of ROS-associated damages in DNA, proteins, and lipids and may result in progressive cell dysfunctions and, in a consequence, apoptosis, increasing the overall probability of an organism's pathological conditions. The superoxide anion is the main undesired by-product of mitochondrial oxidative phosphorylation...
2018: Methods in Molecular Biology
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