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https://www.readbyqxmd.com/read/28529475/fragile-x-associated-tremor-ataxia-syndrome-from-molecular-pathogenesis-to-development-of-therapeutics
#1
REVIEW
Ha Eun Kong, Juan Zhao, Shunliang Xu, Peng Jin, Yan Jin
Fragile X-associated tremor/ataxia syndrome (FXTAS) is a neurodegenerative disorder caused by a premutation CGG repeat expansion (55-200 repeats) within the 5' UTR of the fragile X gene (FMR1). FXTAS is characterized by intension tremor, cerebellar ataxia, progressive neurodegeneration, parkinsonism and cognitive decline. The development of transgenic mouse and Drosophila melanogaster models carrying an expanded CGG repeat has yielded valuable insight into the pathophysiology of FXTAS. To date, we know of two main molecular mechanisms of this disorder: (1) a toxic gain of function of the expanded CGG-repeat FMR1 mRNA, which results in the binding/sequestration of the CGG-binding proteins; and (2) CGG repeat-associated non-AUG-initiated (RAN) translation, which generates a polyglycine peptide toxic to cells...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28512002/cell-surface-g-protein-coupled-receptors-for-tumor-associated-metabolites-a-direct-link-to-mitochondrial-dysfunction-in-cancer
#2
REVIEW
Bojana Ristic, Yangzom D Bhutia, Vadivel Ganapathy
Mitochondria are the sites of pyruvate oxidation, citric acid cycle, oxidative phosphorylation, ketogenesis, and fatty acid oxidation. Attenuation of mitochondrial function is one of the most significant changes that occurs in tumor cells, directly linked to oncogenesis, angiogenesis, Warburg effect, and epigenetics. In particular, three mitochondrial enzymes are inactivated in cancer: pyruvate dehydrogenase (PDH), succinate dehydrogenase (SDH), and 3-hydroxy-3-methylglutaryl CoA synthase-2 (HMGCS2). These enzymes are subject to regulation via acetylation/deacetylation...
May 13, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28502718/mitochondrial-nd5-mutation-mediated-elevated-ros-regulates-apoptotic-pathway-epigenetically-in-a-p53-dependent-manner-for-generating-pro-cancerous-phenotypes
#3
Rajnish Kumar Singh, Sunil Saini, Dileep Verma, Ponnusamy Kalaiarasan, Rameshwar N K Bamezai
We have previously observed concomitant events of mutations in mitochondrial and nuclear genes, along with elevated reactive oxygen species (ROS) and differential methylation within the promoters of nuclear genes in tumors and in vitro experiments of tumorigenesis. These observations have made it pertinent to replicate and understand the role of acquired mitochondrial condition in tuning a cell to accomplish a pro-cancerous state. Using a codon optimized vector system for exogenous over-expression and mitochondrial localization; we have characterized here the role of over-expressed wild type mtND5 and one of its non-synonymous somatic mutation, ND5:P265H...
May 11, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28487205/mitochondrial-determinants-of-cancer-health-disparities
#4
REVIEW
Aaheli Roy Choudhury, Keshav K Singh
Mitochondria are involved in the generation of energy, cell growth and differentiation, cellular signaling, cell cycle control, and cell death. To date, the mitochondrial basis of cancer disparities is unknown. The goal of this review is to provide an understanding and a framework of mitochondrial determinants that may contribute to cancer disparities in racially different populations. Mitochondria, which are multi-functional, have been implicated in the initiation and progression of cancers in relation to metabolic alterations in transformed cells...
May 6, 2017: Seminars in Cancer Biology
https://www.readbyqxmd.com/read/28473874/regional-differences-in-mitochondrial-dna-methylation-in-human-post-mortem-brain-tissue
#5
Matthew Devall, Rebecca G Smith, Aaron Jeffries, Eilis Hannon, Matthew N Davies, Leonard Schalkwyk, Jonathan Mill, Michael Weedon, Katie Lunnon
BACKGROUND: DNA methylation is an important epigenetic mechanism involved in gene regulation, with alterations in DNA methylation in the nuclear genome being linked to numerous complex diseases. Mitochondrial DNA methylation is a phenomenon that is receiving ever-increasing interest, particularly in diseases characterized by mitochondrial dysfunction; however, most studies have been limited to the investigation of specific target regions. Analyses spanning the entire mitochondrial genome have been limited, potentially due to the amount of input DNA required...
2017: Clinical Epigenetics
https://www.readbyqxmd.com/read/28473471/are-targeted-therapies-for-diabetic-cardiomyopathy-on-the-horizon
#6
REVIEW
Mitchel Tate, David J Grieve, Rebecca H Ritchie
Diabetes increases the risk of heart failure approximately 2.5-fold, independent of coronary artery disease and other comorbidities. This process, termed diabetic cardiomyopathy, is characterized by initial impairment of left ventricular (LV) relaxation followed by LV contractile dysfunction. Post-mortem examination reveals that human diastolic dysfunction is closely associated with LV damage, including cardiomyocyte hypertrophy, apoptosis and fibrosis, with impaired coronary microvascular perfusion. The pathophysiological mechanisms underpinning the characteristic features of diabetic cardiomyopathy remain poorly understood, although multiple factors including altered lipid metabolism, mitochondrial dysfunction, oxidative stress, endoplasmic reticulum (ER) stress, inflammation, as well as epigenetic changes, are implicated...
May 1, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28357364/evidence-for-the-hallmarks-of-human-aging-in-replicatively-aging-yeast
#7
REVIEW
Georges E Janssens, Liesbeth M Veenhoff
Recently, efforts have been made to characterize the hallmarks that accompany and contribute to the phenomenon of aging, as most relevant for humans 1. Remarkably, studying the finite lifespan of the single cell eukaryote budding yeast (recently reviewed in 2 and 3) has been paramount for our understanding of aging. Here, we compile observations from literature over the past decades of research on replicatively aging yeast to highlight how the hallmarks of aging in humans are present in yeast. We find strong evidence for the majority of these, and summarize how yeast aging is especially characterized by the hallmarks of genomic instability, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, and mitochondrial dysfunction...
June 20, 2016: Microbial Cell
https://www.readbyqxmd.com/read/28357065/role-of-micrornas-in-the-pathogenesis-of-diabetic-cardiomyopathy
#8
Xinyu Liu, Shixue Liu
The morbidity of diabetes mellitus has been increasing annually. As a progressive metabolic disorder, chronic complications occur in the late stage of diabetes. In addition, cardiovascular diseases account for the major cause of morbidity and mortality among the diabetic population worldwide. Diabetic cardiomyopathy (DCM) is a type of diabetic heart disease. Patients with DCM show symptoms and signs of heart failure while no specific cause, such as coronary disease, hypertension, alcohol consumption, or other structural heart diseases has been identified...
February 2017: Biomedical Reports
https://www.readbyqxmd.com/read/28347844/complex-inhibition-of-autophagy-by-mitochondrial-aldehyde-dehydrogenase-shortens-lifespan-and-exacerbates-cardiac-aging
#9
Yingmei Zhang, Cong Wang, Jingmin Zou, Aijun Sun, Lindsay K Hueckstaedt, Junbo Ge, Jun Ren
Autophagy, a conservative degradation process for long-lived and damaged proteins, participates in a cascade of biological processes including aging. A number of autophagy regulators have been identified. Here we demonstrated that mitochondrial aldehyde dehydrogenase (ALDH2), an enzyme with the most common single point mutation in humans, governs cardiac aging through regulation of autophagy. Myocardial mechanical and autophagy properties were examined in young (4 mo) and old (26-28 mo) wild-type (WT) and global ALDH2 transgenic mice...
March 24, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28333387/pathophysiological-fundamentals-of-diabetic-cardiomyopathy
#10
Xinyue Hu, Tao Bai, Zheng Xu, Qiuju Liu, Yang Zheng, Lu Cai
Diabetic cardiomyopathy (DCM) was first recognized more than four decades ago and occurred independent of cardiovascular diseases or hypertension in both type 1 and type 2 diabetic patients. The exact mechanisms underlying this disease remain incompletely understood. Several pathophysiological bases responsible for DCM have been proposed, including the presence of hyperglycemia, nonenzymatic glycosylation of large molecules (e.g., proteins), energy metabolic disturbance, mitochondrial damage and dysfunction, impaired calcium handling, reactive oxygen species formation, inflammation, cardiac cell death, and cardiac hypertrophy and fibrosis, leading to impairment of cardiac contractile functions...
March 16, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28253983/micrornas-aging-cellular-senescence-and-alzheimer-s-disease
#11
P H Reddy, J Williams, F Smith, J S Bhatti, S Kumar, M Vijayan, R Kandimalla, C S Kuruva, R Wang, M Manczak, X Yin, A P Reddy
Aging is a normal process of living being. It has been reported that multiple cellular changes, including oxidative damage/mitochondrial dysfunction, telomere shortening, inflammation, may accelerate the aging process, leading to cellular senescence. These cellular changes induce age-related human diseases, including Alzheimer's, Parkinson's, multiple sclerosis, amyotrophic lateral sclerosis, cardiovascular, cancer, and skin diseases. Changes in somatic and germ-line DNA and epigenetics are reported to play large roles in accelerating the onset of human diseases...
2017: Progress in Molecular Biology and Translational Science
https://www.readbyqxmd.com/read/28219123/identification-of-core-gene-networks-and-hub-genes-associated-with-progression-of-non-alcoholic-fatty-liver-disease-by-rna-sequencing
#12
Kikuko Hotta, Masataka Kikuchi, Takuya Kitamoto, Aya Kitamoto, Yuji Ogawa, Yasushi Honda, Takaomi Kessoku, Kaori Kobayashi, Masato Yoneda, Kento Imajo, Wataru Tomeno, Akihiro Nakaya, Yutaka Suzuki, Satoru Saito, Atsushi Nakajima
AIM: Non-alcoholic fatty liver disease (NAFLD) progresses because of the interaction between numerous genes. Thus, we carried out a weighted gene coexpression network analysis to identify core gene networks and key genes associated with NAFLD progression. METHODS: We enrolled 39 patients with mild NAFLD (fibrosis stages 0-2) and 21 with advanced NAFLD (fibrosis stages 3-4). Total RNA was extracted from frozen liver biopsies, and sequenced to capture a large dynamic range of expression levels...
February 20, 2017: Hepatology Research: the Official Journal of the Japan Society of Hepatology
https://www.readbyqxmd.com/read/28188297/alternative-splicing-in-the-cytochrome-p450-superfamily-expands-protein-diversity-to-augment-gene-function-and-redirect-human-drug-metabolism
#13
Andrew J Annalora, Craig B Marcus, Patrick L Iversen
The human genome encodes 57 cytochrome P450 (CYP) genes whose enzyme products metabolize hundreds of drugs, thousands of xenobiotics and unknown numbers of endogenous compounds including steroids, retinoids and icosinoids. Indeed, CYP genes are the first line of defense against daily environmental chemical challenges in a manner that parallels the immune system. Several databases, including PubMed, AceView, and Ensembl, were queried to establish a comprehensive analysis of the full human CYP transcriptome. This review describes a remarkable diversification of the 57 human CYP genes, which may be alternatively processed into nearly 1000 distinct mRNA transcripts to shape an individual's CYP proteome...
February 10, 2017: Drug Metabolism and Disposition: the Biological Fate of Chemicals
https://www.readbyqxmd.com/read/28185716/mitochondrial-complex-ii-at-the-crossroads
#14
REVIEW
Ayenachew Bezawork-Geleta, Jakub Rohlena, Lanfeng Dong, Karel Pacak, Jiri Neuzil
Mitochondrial complex II (CII), also called succinate dehydrogenase (SDH), is a central purveyor of the reprogramming of metabolic and respiratory adaptation in response to various intrinsic and extrinsic stimuli and abnormalities. In this review we discuss recent findings regarding SDH biogenesis, which requires four known assembly factors, and modulation of its enzymatic activity by acetylation, succinylation, phosphorylation, and proteolysis. We further focus on the emerging role of both genetic and epigenetic aberrations leading to SDH dysfunction associated with various clinical manifestations...
February 6, 2017: Trends in Biochemical Sciences
https://www.readbyqxmd.com/read/28012783/epigenetic-regulation-of-redox-signaling-in-diabetic-retinopathy-role-of-nrf2
#15
REVIEW
Renu A Kowluru, Manish Mishra
Diabetic retinopathy is a major vision threatening disease among working age adults, and increased oxidative stress is one of the prime causative factors in its pathogenesis. Increased reactive oxygen species (ROS) in the cytosol damage mitochondria, and due to compromised antioxidant signaling system and dysfunctional mitochondria with damaged mitochondrial DNA, ROS continue to pile up, accelerating capillary cell loss. In addition to other cellular and enzymatic defense systems, the retina is also equipped with the nuclear erythroid-2-p45-related factor-2 (Nrf2) antioxidant response element signaling pathway, which controls the expression of genes important in detoxification and elimination of ROS...
February 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28003373/chronic-inflammation-accelerator-of-biological-aging
#16
REVIEW
Bertrand Fougère, Eric Boulanger, Fati Nourhashémi, Sophie Guyonnet, Matteo Cesari
Biological aging is characterized by a chronic low-grade inflammation level. This chronic phenomenon has been named "inflamm-aging" and is a highly significant risk factor for morbidity and mortality in the older persons. The most common theories of inflamm-aging include redox stress, mitochondrial dysfunction, glycation, deregulation of the immune system, hormonal changes, epigenetic modifications, and dysfunction telomere attrition. Inflamm-aging plays a role in the initiation and progression of age-related diseases such as type II diabetes, Alzheimer's disease, cardiovascular disease, frailty, sarcopenia, osteoporosis, and cancer...
December 21, 2016: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
https://www.readbyqxmd.com/read/27959617/senescence-in-copd-and-its-comorbidities
#17
Peter J Barnes
Chronic obstructive pulmonary disease (COPD) is regarded as a disease of accelerated lung aging. This affliction shows all of the hallmarks of aging, including telomere shortening, cellular senescence, activation of PI3 kinase-mTOR signaling, impaired autophagy, mitochondrial dysfunction, stem cell exhaustion, epigenetic changes, abnormal microRNA profiles, immunosenescence, and a low-grade chronic inflammation (inflammaging). Many of these pathways are driven by chronic exogenous and endogenous oxidative stress...
February 10, 2017: Annual Review of Physiology
https://www.readbyqxmd.com/read/27922198/dnmt1-modulation-in-chronic-hepatitis-b-patients-and-hypothetic-influence-on-mitochondrial-dna-methylation-status-during-long-term-nucleo-t-side-analogs-therapy
#18
Giordano Madeddu, Silvia Ortu, Giovanni Garrucciu, Ivana Maida, Michela Melis, Alberto Augusto Muredda, Maria Stella Mura, Sergio Babudieri
Inhibition of viral replication is the most important goal in patients with Hepatitis B virus chronic infection (CHB). Currently, five oral nucleo(t)side analogs (NAs), including Lamivudine, Adefovir, Telbivudine, Entecavir, and Tenofovir, have been approved for treatment. The widespread use of NAs has also been linked with a progressive growth of unlikely anomaly attributable to mitochondrial dysfunctions, not previously recognized. Here, we explore the hypothesis that NAs may cause persistent epigenetic changes during prolonged NAs therapy in CHB patients...
July 2017: Journal of Medical Virology
https://www.readbyqxmd.com/read/27816931/underlying-role-of-mitochondrial-mutagenesis-in-the-pathogenesis-of-a-disease-and-current-approaches-for-translational-research
#19
Maria Paraskevaidi, Pierre L Martin-Hirsch, Maria Kyrgiou, Francis L Martin
Mitochondrial diseases have been extensively investigated over the last three decades, but many questions regarding their underlying aetiologies remain unanswered. Mitochondrial dysfunction is not only responsible for a range of neurological and myopathy diseases but also considered pivotal in a broader spectrum of common diseases such as epilepsy, autism and bipolar disorder. These disorders are a challenge to diagnose and treat, as their aetiology might be multifactorial. In this review, the focus is placed on potential mechanisms capable of introducing defects in mitochondria resulting in disease...
May 1, 2017: Mutagenesis
https://www.readbyqxmd.com/read/27794418/sirt3-deficiency-exacerbates-diabetic-cardiac-dysfunction-role-of-foxo3a-parkin-mediated-mitophagy
#20
REVIEW
Wenjun Yu, Beilei Gao, Na Li, Jiaxing Wang, Cuiting Qiu, Guoyong Zhang, Min Liu, Rongqing Zhang, Congye Li, Gang Ji, Yingmei Zhang
Diabetic cardiomyopathy (DCM) is often associated with suppressed cardiac autophagy, mitochondrial structural and functional impairment. Sirtuin-3 (Sirt3) has been reported to play a crucial role in mitochondrial homeostasis and confers a protective role against the onset and development of DCM although the precise mechanism(s) remains elusive. Here we hypothesized that Sirt3 exerts cardioprotection against DCM by activating Parkin-mediated mitophagy, en route to preserved mitochondrial homeostasis and suppressed cardiomyocyte apoptosis...
October 26, 2016: Biochimica et Biophysica Acta
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