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(Epigenetic) and (mitochondrial dysfunction)

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https://www.readbyqxmd.com/read/29118760/septic-shock-and-the-aging-process-a-molecular-comparison
#1
Fabiano Pinheiro da Silva, Marcel Cerqueira César Machado
Aging is a continuous process promoted by both intrinsic and extrinsic factors that each trigger a multitude of molecular events. Increasing evidence supports a central role for inflammation in this progression. Here, we discuss how the low-grade chronic inflammation that characterizes aging is tightly interconnected with other important aspects of this process, such as DNA damage, mitochondrial dysfunction, and epigenetic changes. Similarly, inflammation also plays a critical role in many morbid conditions that affect patients who are admitted to Intensive Care...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/29110598/sirt1-as-a-therapeutic-target-in-diabetic-complications
#2
Justyna Strycharz, Żaneta Rygielska, Ewa Świderska, Józef Drzewoski, Janusz Szemraj, Leszek Szmigiero, Agnieszka Śliwińska
Background SIRT1 is an epigenetic enzyme involved in histone and non-histone protein deacetylation. It acts primarily as a metabolic sensor, which responses to changing energy status by deacetylating crucial transcription factors and cofactors. In this way, SIRT1 regulates mitochondrial function and biogenesis, oxidative stress, inflammation, apoptosis and cellular senescence. Disturbance of all of these phenomena promotes the pathogenesis of diabetic complications. These disorders are inseparably connected with chronic hyperglycemia, which possesses a strong epigenetic determinant...
November 6, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/29073779/mitochondrial-nad-nadh-redox-state-and-diabetic-cardiomyopathy
#3
Jessica M Berthiaume, Jacob G Kurdys, Danina M Muntean, Mariana G Rosca
SIGNIFICANCE: Diabetic cardiomyopathy is a frequent complication occurring even in well-controlled asymptomatic diabetic patients, and may advance to heart failure. Recent advances: The diabetic heart is characterized by a state of "metabolic rigidity" involving enhanced rates of fatty acid uptake and mitochondrial oxidation as the predominant energy source, and exhibits mitochondrial electron transport chain defects. These alterations promote redox state changes evidenced by a decreased NAD+/NADH ratio associated with an increase in acetyl-CoA/CoA ratio...
October 26, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/29059699/identification-of-the-genomic-region-under-epigenetic-regulation-during-nonalcoholic-fatty-liver-disease-progression
#4
Kikuko Hotta, Takuya Kitamoto, Aya Kitamoto, Yuji Ogawa, Yasushi Honda, Takaomi Kessoku, Masato Yoneda, Kento Imajo, Wataru Tomeno, Satoru Saito, Atsushi Nakajima
AIM: The progression of nonalcoholic fatty liver disease (NAFLD) is affected by epigenetics. We performed co-methylation and differentially methylated region (DMR) analyses to identify the genomic region that is under epigenetic regulation during NAFLD progression. METHODS: We collected liver biopsy specimens from 60 Japanese patients with NAFLD and classified these into mild (fibrosis stages 0-2) or advanced (fibrosis stages 3-4) NAFLD. We performed genome-wide DNA methylation analysis and identified the differentially methylated CpGs between mild and advanced NAFLD...
October 23, 2017: Hepatology Research: the Official Journal of the Japan Society of Hepatology
https://www.readbyqxmd.com/read/29043077/recent-advances-in-understanding-werner-syndrome
#5
REVIEW
Raghavendra A Shamanna, Deborah L Croteau, Jong-Hyuk Lee, Vilhelm A Bohr
Aging, the universal phenomenon, affects human health and is the primary risk factor for major disease pathologies. Progeroid diseases, which mimic aging at an accelerated rate, have provided cues in understanding the hallmarks of aging. Mutations in DNA repair genes as well as in telomerase subunits are known to cause progeroid syndromes. Werner syndrome (WS), which is characterized by accelerated aging, is an autosomal-recessive genetic disorder. Hallmarks that define the aging process include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulation of nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication...
2017: F1000Research
https://www.readbyqxmd.com/read/29027980/the-plasticizer-bisphenol-a-perturbs-the-hepatic-epigenome-a-systems-level-analysis-of-the-mirnome
#6
Ludivine Renaud, Willian A da Silveira, E Starr Hazard, Jonathan Simpson, Silvia Falcinelli, Dongjun Chung, Oliana Carnevali, Gary Hardiman
Ubiquitous exposure to bisphenol A (BPA), an endocrine disruptor (ED), has raised concerns for both human and ecosystem health. Epigenetic factors, including microRNAs (miRNAs), are key regulators of gene expression during cancer. The effect of BPA exposure on the zebrafish epigenome remains poorly characterized. Zebrafish represents an excellent model to study cancer as the organism develops a disease that resembles human cancer. Using zebrafish as a systems toxicology model, we hypothesized that chronic BPA-exposure impacts the miRNome in adult zebrafish and establishes an epigenome more susceptible to cancer development...
October 13, 2017: Genes
https://www.readbyqxmd.com/read/29018509/circrna_0046367-prevents-hepatoxicity-of-lipid-peroxidation-an-inhibitory-role-against-hepatic-steatosis
#7
Xing-Ya Guo, Jian-Neng Chen, Fang Sun, Yu-Qin Wang, Qin Pan, Jian-Gao Fan
Hepatic steatosis reflects the miRNA-related pathological disorder with triglyceride accumulation and lipid peroxidation, which leads to nonalcoholic steatohepatitis, liver fibrosis/cirrhosis, and even hepatocellular carcinoma. Circular RNA (circRNA)/miRNA interaction reveals a novel layer of epigenetic regulation, yet the miRNA-targeting circRNA remains uncertain in hepatic steatosis. Here, we uncover circRNA_0046367 to be endogenous modulator of miR-34a that underlies hepatic steatosis. In contrast to its expression loss during the hepatocellular steatosis in vivo and in vitro, circRNA_0046367 normalization abolished miR-34a's inhibitory effect on peroxisome proliferator-activated receptor α (PPARα) via blocking the miRNA/mRNA interaction with miRNA response elements (MREs)...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29016348/parp-1-and-parp-2-activity-in-cancer-induced-cachexia-potential-therapeutic-implications
#8
Esther Barreiro, Joaquim Gea
Skeletal muscle dysfunction and mass loss is a characteristic feature in patients with chronic diseases including cancer and acute conditions such as critical illness. Maintenance of an adequate muscle mass is crucial for the patients' prognosis irrespective of the underlying condition. Moreover, aging-related sarcopenia may further aggravate the muscle wasting process associated with chronic diseases and cancer. Poly(adenosine diphosphate-ribose) polymerase (PARP) activation has been demonstrated to contribute to the pathophysiology of muscle mass loss and dysfunction in animal models of cancer-induced cachexia...
October 26, 2017: Biological Chemistry
https://www.readbyqxmd.com/read/28986361/regulating-microrna-expression-at-the-heart-of-diabetes-mellitus-and-the-mitochondrion
#9
Quincy A Hathaway, Mark V Pinti, Andrya J Durr, Shanawar Waris, Danielle L Shepherd, John M Hollander
Type 2 diabetes mellitus is a major risk factor for cardiovascular disease and mortality. Uncontrolled type 2 diabetes mellitus results in a systemic milieu of increased circulating glucose and fatty acids. The development of insulin resistance in cardiac tissue decreases cellular glucose import and enhances mitochondrial fatty acid uptake. While triacylglycerol and cytotoxic lipid species begin to accumulate in the cardiomyocyte, the energy substrate utilization ratio of free fatty acids (FFAs) to glucose changes to almost entirely FFAs...
October 6, 2017: American Journal of Physiology. Heart and Circulatory 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
#10
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...
November 2017: Ageing Research Reviews
https://www.readbyqxmd.com/read/28983101/emerging-therapies-for-idiopathic-pulmonary-fibrosis-a-progressive-age-related-disease
#11
REVIEW
Ana L Mora, Mauricio Rojas, Annie Pardo, Moises Selman
Idiopathic pulmonary fibrosis (IPF) is a fatal age-associated disease that is characterized by progressive and irreversible scarring of the lung. The pathogenesis of IPF is not completely understood and current therapies are limited to those that reduce the rate of functional decline in patients with mild-to-moderate disease. In this context, new therapeutic approaches that substantially improve the survival time and quality of life of these patients are urgently needed. Our incomplete understanding of the pathogenic mechanisms of IPF and the lack of appropriate experimental models that reproduce the key characteristics of the human disease are major challenges...
November 2017: Nature Reviews. Drug Discovery
https://www.readbyqxmd.com/read/28965985/dysfunctions-of-mitochondria-in-close-association-with-strong-perturbation-of-long-noncoding-rnas-expression-in-down-syndrome
#12
Jia-Jun Qiu, Yan-Na Liu, Zhao-Rui Ren, Jing-Bin Yan
Trisomy 21 is the most common chromosomal disorder and underlies Down syndrome. Epigenetics, such as DNA methylation and post-translational histone modifications, plays a vital role in Down syndrome. However, the functions of epigenetics-related long noncoding RNAs (lncRNAs), found to have an impact on neural diseases such as Alzheimer's disease, remain unknown in Down syndrome. In this study, we analyzed the RNA sequencing data from Down syndrome-induced pluripotent stem cells (iPSCs) and normal iPSCs. A large number of lncRNAs were identified differentially expressed in Down syndrome-iPSCs...
September 29, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28949008/vitamin-d-deficiency-accelerates-ageing-and-age-related-diseases-a-novel-hypothesis
#13
Michael J Berridge
Ageing can occur at different rates, but what controls this variable rate is unknown. Here I have developed a hypothesis that vitamin D may act to control the rate of ageing. The basis of this hypothesis emerged from studyng the various cellular processes that control ageing. These processes such as autophagy, mitochondrial dysfunction, inflammation, oxidative stress, epigenetic changes, DNA disorders and alterations in Ca(2+) and reactive oxygen species (ROS) signalling are all known to be regulated by vitamin D...
November 15, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28941093/staging-in-bipolar-disorder-from-theoretical-framework-to-clinical-utility
#14
Michael Berk, Robert Post, Aswin Ratheesh, Emma Gliddon, Ajeet Singh, Eduard Vieta, Andre F Carvalho, Melanie M Ashton, Lesley Berk, Susan M Cotton, Patrick D McGorry, Brisa S Fernandes, Lakshmi N Yatham, Seetal Dodd
Illness staging is widely utilized in several medical disciplines to help predict course or prognosis, and optimize treatment. Staging models in psychiatry in general, and bipolar disorder in particular, depend on the premise that psychopathology moves along a predictable path: an at-risk or latency stage, a prodrome progressing to a first clinical threshold episode, and one or more recurrences with the potential to revert or progress to late or end-stage manifestations. The utility and validity of a staging model for bipolar disorder depend on its linking to clinical outcome, treatment response and neurobiological measures...
October 2017: World Psychiatry: Official Journal of the World Psychiatric Association (WPA)
https://www.readbyqxmd.com/read/28865727/altered-mitochondrial-epigenetics-associated-with-subchronic-doxorubicin-cardiotoxicity
#15
André Ferreira, Teresa Cunha-Oliveira, Rui F Simões, Filipa S Carvalho, Ana Burgeiro, Kendra Nordgren, Kendall B Wallace, Paulo J Oliveira
Doxorubicin (DOX), a potent and broad-spectrum antineoplastic agent, causes an irreversible, cumulative and dose-dependent cardiomyopathy that ultimately leads to congestive heart failure. The mechanisms responsible for DOX cardiotoxicity remain poorly understood, but seem to involve mitochondrial dysfunction on several levels. Epigenetics may explain a portion of this effect. Since mitochondrial dysfunction may affect the epigenetic landscape, we hypothesize that this cardiac toxicity may result from epigenetic changes related to disruption of mitochondrial function...
September 1, 2017: Toxicology
https://www.readbyqxmd.com/read/28855114/mitochondrial-epigenetic-crosstalk-in-environmental-toxicology
#16
Caren Weinhouse
Crosstalk between the nuclear epigenome and mitochondria, both in normal physiological function and in responses to environmental toxicant exposures, is a developing sub-field of interest in environmental and molecular toxicology. The majority (∼99%) of mitochondrial proteins are encoded in the nuclear genome, so programmed communication among nuclear, cytoplasmic, and mitochondrial compartments is essential for maintaining cellular health. In this review, we will focus on correlative and mechanistic evidence for direct impacts of each system on the other, discuss demonstrated or potential crosstalk in the context of chemical insult, and highlight biological research questions for future study...
November 1, 2017: Toxicology
https://www.readbyqxmd.com/read/28822233/obese-fathers-lead-to-an-altered-metabolism-and-obesity-in-their-children-in-adulthood-review-of-experimental-and-human-studies
#17
REVIEW
Fernanda Ornellas, Priscila V Carapeto, Carlos A Mandarim-de-Lacerda, Marcia B Aguila
OBJECTIVE: To discuss the recent literature on paternal obesity, focusing on the possible mechanisms of transmission of the phenotypes from the father to the children. SOURCES: A non-systematic review in the PubMed database found few publications in which paternal obesity was implicated in the adverse transmission of characteristics to offspring. Specific articles on epigenetics were also evaluated. As the subject is recent and still controversial, all articles were considered regardless of year of publication...
August 17, 2017: Jornal de Pediatria
https://www.readbyqxmd.com/read/28809938/perinatal-testosterone-exposure-potentiates-vascular-dysfunction-by-er%C3%AE-suppression-in-endothelial-progenitor-cells
#18
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/28760656/norcantharidin-induces-mitochondrial-dependent-apoptosis-through-mcl-1-inhibition-in-human-prostate-cancer-cells
#19
Chu-Liang Lin, Chien-Min Chen, Chia-Liang Lin, Chun-Wen Cheng, Chien-Hsing Lee, Yi-Hsien Hsieh
Norcantharidin (NCTD) is the demethylated form of cantharidin that exhibits anticancer potential in many cancer cell types. Recent reports suggest that NCTD targeting ROS/AMPK and DNA replication signaling pathway could be an effective strategy for the treatment of PCa cells. However, supportive evidence is limited to the effect of NCTD that induction of apoptosis through suppression of the Mcl-1. Here, we show that NCTD induced PCa cell apoptosis and triggered caspase activation, which was associated with mitochondria dysfunction...
July 29, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28752219/the-putative-role-of-environmental-aluminium-in-the-development-of-chronic-neuropathology-in-adults-and-children-how-strong-is-the-evidence-and-what-could-be-the-mechanisms-involved
#20
REVIEW
Gerwyn Morris, Basant K Puri, Richard E Frye
The conceptualisation of autistic spectrum disorder and Alzheimer's disease has undergone something of a paradigm shift in recent years and rather than being viewed as single illnesses with a unitary pathogenesis and pathophysiology they are increasingly considered to be heterogeneous syndromes with a complex multifactorial aetiopathogenesis, involving a highly complex and diverse combination of genetic, epigenetic and environmental factors. One such environmental factor implicated as a potential cause in both syndromes is aluminium, as an element or as part of a salt, received, for example, in oral form or as an adjuvant...
July 27, 2017: Metabolic Brain Disease
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