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Telomere and fibrosis

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https://www.readbyqxmd.com/read/28799249/opposing-effects-on-cardiac-function-by-calorie-restriction-in-different-aged-mice
#1
Yunlu Sheng, Shan Lv, Min Huang, Yifan Lv, Jing Yu, Juan Liu, Tingting Tang, Hanmei Qi, Wenjuan Di, Guoxian Ding
Calorie restriction (CR) increases average and maximum lifespan and exhibits an apparent beneficial impact on age-related diseases. Several studies have shown that CR initiated either in middle or old age could improve ischemic tolerance and rejuvenate the aging heart; however, the data are not uniform when initiated in young. The accurate time to initiate CR providing maximum benefits for cardiac remodeling and function during aging remains unclear. Thus, whether a similar degree of CR initiated in mice of different ages could exert a similar effect on myocardial protection was investigated in this study...
August 11, 2017: Aging Cell
https://www.readbyqxmd.com/read/28665427/effects-of-bioactive-compounds-on-senescence-and-components-of-senescence-associated-secretory-phenotypes-in-vitro
#2
REVIEW
Janubová Mária, Žitňanová Ingrid
Senescence is a permanent cell cycle arrest that is accompanied by changes in cell morphology and physiology occurring in vitro and in vivo. Senescence evolved as a beneficial response to damage promoting wound healing, limiting fibrosis, fighting against cancer and helping embryonic development. However, excessive accumulation of senescent cells is considered to play a substantial role in the development of aging-related diseases and other morphological and physiological changes associated with aging. Therefore, the aim of many researchers is to find out a way to eliminate senescent cells and improve the health condition of aging people...
July 19, 2017: Food & Function
https://www.readbyqxmd.com/read/28665198/whole-exome-sequencing-insights-into-adult-pulmonary-fibrosis-repeating-the-telomere-theme
#3
Christine Kim Garcia
No abstract text is available yet for this article.
July 1, 2017: American Journal of Respiratory and Critical Care Medicine
https://www.readbyqxmd.com/read/28659816/cardioprotective-effects-of-sirt6-in-a-mouse-model-of-transverse-aortic-constriction-induced-heart-failure
#4
Yongming Li, Xianda Meng, Wenguang Wang, Fu Liu, Zhiru Hao, Yang Yang, Jinbo Zhao, Wensi Yin, Lijuan Xu, Ruiping Zhao, Jiang Hu
SIRT6, a member of the NAD (+)-dependent class III deacetylase sirtuin family, plays important roles in the maintenance of cardiovascular homeostasis. Telomere shortening is a risk factor for age-associated diseases, including heart disease. In the present study, we investigated the role of SIRT6 and telomerase in a mouse model of transverse aortic constriction (TAC)-induced heart failure. SIRT6, telomerase reverse transcriptase (TERT), and telomere repeat binding factor (TRF)-1 were significantly downregulated in TAC mice compared with their expression in sham-operated mice...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28648751/the-muc5b-promoter-polymorphism-and-telomere-length-in-patients-with-chronic-hypersensitivity-pneumonitis-an-observational-cohort-control-study
#5
Brett Ley, Chad A Newton, Isabel Arnould, Brett M Elicker, Travis S Henry, Eric Vittinghoff, Jeffrey A Golden, Kirk D Jones, Kiran Batra, Jose Torrealba, Christine Kim Garcia, Paul J Wolters
BACKGROUND: Patients with hypersensitivity pneumonitis are at risk of developing pulmonary fibrosis, which is associated with reduced survival. In families with multiple affected members, individuals might be diagnosed as having idiopathic pulmonary fibrosis (IPF) or chronic (fibrotic) hypersensitivity pneumonitis, which suggests these disorders share risk factors. We aimed to test whether the genomic risk factors associated with the development and progression of IPF are also associated with the development of fibrosis and reduced survival in people with chronic hypersensitivity pneumonitis...
August 2017: Lancet Respiratory Medicine
https://www.readbyqxmd.com/read/28637614/classical-inherited-bone-marrow-failure-syndromes-with-high-risk-for-myelodysplastic-syndrome-and-acute-myelogenous-leukemia
#6
REVIEW
Sharon A Savage, Carlo Dufour
The inherited marrow failure syndromes (IBMFS) are a heterogeneous group of diseases characterized by failure in the production of one or more blood lineage. The clinical manifestations of the IBMFS vary according to the type and number of blood cell lines involved, including different combinations of anemia, leukopenia, and thrombocytopenia. In some IBMFS, systemic non-hematologic manifestations, including congenital malformations, mucocutaneous abnormalities, developmental delay, and other medical complications, may be present...
April 2017: Seminars in Hematology
https://www.readbyqxmd.com/read/28507545/clinical-and-molecular-heterogeneity-of-rtel1-deficiency
#7
Carsten Speckmann, Sushree Sangita Sahoo, Marta Rizzi, Shinsuke Hirabayashi, Axel Karow, Nina Kathrin Serwas, Marc Hoemberg, Natalja Damatova, Detlev Schindler, Jean-Baptiste Vannier, Simon J Boulton, Ulrich Pannicke, Gudrun Göhring, Kathrin Thomay, J J Verdu-Amoros, Holger Hauch, Wilhelm Woessmann, Gabriele Escherich, Eckart Laack, Liliana Rindle, Maximilian Seidl, Anne Rensing-Ehl, Ekkehart Lausch, Christine Jandrasits, Brigitte Strahm, Klaus Schwarz, Stephan R Ehl, Charlotte Niemeyer, Kaan Boztug, Marcin W Wlodarski
Typical features of dyskeratosis congenita (DC) resulting from excessive telomere shortening include bone marrow failure (BMF), mucosal fragility, and pulmonary or liver fibrosis. In more severe cases, immune deficiency and recurring infections can add to disease severity. RTEL1 deficiency has recently been described as a major genetic etiology, but the molecular basis and clinical consequences of RTEL1-associated DC are incompletely characterized. We report our observations in a cohort of six patients: five with novel biallelic RTEL1 mutations p...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28495692/shared-genetic-predisposition-in-rheumatoid-arthritis-interstitial-lung-disease-and-familial-pulmonary-fibrosis
#8
Pierre-Antoine Juge, Raphaël Borie, Caroline Kannengiesser, Steven Gazal, Patrick Revy, Lidwine Wemeau-Stervinou, Marie-Pierre Debray, Sébastien Ottaviani, Sylvain Marchand-Adam, Nadia Nathan, Gabriel Thabut, Christophe Richez, Hilario Nunes, Isabelle Callebaut, Aurélien Justet, Nicolas Leulliot, Amélie Bonnefond, David Salgado, Pascal Richette, Jean-Pierre Desvignes, Huguette Lioté, Philippe Froguel, Yannick Allanore, Olivier Sand, Claire Dromer, René-Marc Flipo, Annick Clément, Christophe Béroud, Jean Sibilia, Baptiste Coustet, Vincent Cottin, Marie-Christophe Boissier, Benoit Wallaert, Thierry Schaeverbeke, Florence Dastot le Moal, Aline Frazier, Christelle Ménard, Martin Soubrier, Nathalie Saidenberg, Dominique Valeyre, Serge Amselem, Catherine Boileau, Bruno Crestani, Philippe Dieudé
Despite its high prevalence and mortality, little is known about the pathogenesis of rheumatoid arthritis-associated interstitial lung disease (RA-ILD). Given that familial pulmonary fibrosis (FPF) and RA-ILD frequently share the usual pattern of interstitial pneumonia and common environmental risk factors, we hypothesised that the two diseases might share additional risk factors, including FPF-linked genes. Our aim was to identify coding mutations of FPF-risk genes associated with RA-ILD.We used whole exome sequencing (WES), followed by restricted analysis of a discrete number of FPF-linked genes and performed a burden test to assess the excess number of mutations in RA-ILD patients compared to controls...
May 2017: European Respiratory Journal: Official Journal of the European Society for Clinical Respiratory Physiology
https://www.readbyqxmd.com/read/28456362/pericardial-interstitial-cell-senescence-responsible-for-pericardial-structural-remodeling-in-idiopathic-and-postsurgical-constrictive-pericarditis
#9
Lin Han, Xin Li, Guanxin Zhang, Zhiyun Xu, Dejun Gong, Fanglin Lu, Xiaohong Liu
OBJECTIVE: Idiopathic and postsurgical constrictive pericarditis is characterized by pericardial structural remodeling that involves fibrosis, calcification, and inflammation. This study aimed to determine whether cell senescence was responsible for pericardial structural remodeling. METHODS: Pericardial interstitial cells derived from patients with idiopathic or postsurgical pericarditis (pericarditis cells) were harvested. Timing of senescence and differences in telomere length were compared between age- and sex-matched controls (nonpericarditis cells)...
April 4, 2017: Journal of Thoracic and Cardiovascular Surgery
https://www.readbyqxmd.com/read/28446600/management-of-suspected-monogenic-lung-fibrosis-in-a-specialised-centre
#10
Raphael Borie, Caroline Kannengiesser, Flore Sicre de Fontbrune, Laurent Gouya, Nadia Nathan, Bruno Crestani
At least 10% of patients with interstitial lung disease present monogenic lung fibrosis suspected on familial aggregation of pulmonary fibrosis, specific syndromes or early age of diagnosis. Approximately 25% of families have an identified mutation in genes mostly involved in telomere homeostasis, and more rarely in surfactant homeostasis.Beyond pathophysiological knowledge, detection of these mutations has practical consequence for patients. For instance, mutations involved in telomere homeostasis are associated with haematological complications after lung transplantation and may require adapted immunosuppression...
June 30, 2017: European Respiratory Review: An Official Journal of the European Respiratory Society
https://www.readbyqxmd.com/read/28431248/spontaneous-chitin-accumulation-in-airways-and-age-related-fibrotic-lung-disease
#11
Steven J Van Dyken, Hong-Erh Liang, Ram P Naikawadi, Prescott G Woodruff, Paul J Wolters, David J Erle, Richard M Locksley
The environmentally widespread polysaccharide chitin is degraded and recycled by ubiquitous bacterial and fungal chitinases. Although vertebrates express active chitinases from evolutionarily conserved loci, their role in mammalian physiology is unclear. We show that distinct lung epithelial cells secrete acidic mammalian chitinase (AMCase), which is required for airway chitinase activity. AMCase-deficient mice exhibit premature morbidity and mortality, concomitant with accumulation of environmentally derived chitin polymers in the airways and expression of pro-fibrotic cytokines...
April 20, 2017: Cell
https://www.readbyqxmd.com/read/28373051/telomere-length-profiles-in-primary-human-peritoneal-mesothelial-cells-are-consistent-with-senescence
#12
Melisa Lopez-Anton, András Rudolf, Duncan M Baird, Laureline Roger, Rhiannon E Jones, Janusz Witowski, Donald J Fraser, Timothy Bowen
Mesothelial cell (MC) senescence contributes to malignancy and tissue fibrosis. The role of telomere erosion in MC senescence remains controversial, with evidence for both telomere-dependent and telomere-independent mechanisms reported. Single telomere length analysis revealed considerable telomere length heterogeneity in freshly isolated human peritoneal MCs, reflecting a heterogeneous proliferative history and providing high-resolution evidence for telomere-dependent senescence. By contrast the attenuated replicative lifespan, lack of telomere erosion and induction of p16 expression in in vitro-aged cells was consistent with stress-induced senescence...
April 1, 2017: Mechanisms of Ageing and Development
https://www.readbyqxmd.com/read/28318743/broadening-the-investigation-short-telomeres-and-lung-transplantation-outcomes-in-pulmonary-fibrosis
#13
EDITORIAL
Andrew Courtwright, Souheil El-Chemaly
No abstract text is available yet for this article.
February 28, 2017: Journal of Heart and Lung Transplantation
https://www.readbyqxmd.com/read/28289249/control-of-cellular-aging-tissue-function-and-cancer-by-p53-downstream-of-telomeres
#14
REVIEW
Caitlin M Roake, Steven E Artandi
Telomeres, the nucleoprotein complex at the ends of eukaryotic chromosomes, perform an essential cellular role in part by preventing the chromosomal end from initiating a DNA-damage response. This function of telomeres can be compromised as telomeres erode either as a consequence of cell division in culture or as a normal part of cellular ageing in proliferative tissues. Telomere dysfunction in this context leads to DNA-damage signaling and activation of the tumor-suppressor protein p53, which then can prompt either cellular senescence or apoptosis...
May 1, 2017: Cold Spring Harbor Perspectives in Medicine
https://www.readbyqxmd.com/read/28262440/telomere-length-in-patients-with-pulmonary-fibrosis-associated-with-chronic-lung-allograft-dysfunction-and-post-lung-transplantation-survival
#15
Chad A Newton, Julia Kozlitina, Jefferson R Lines, Vaidehi Kaza, Fernando Torres, Christine Kim Garcia
BACKGROUND: Prior studies have shown that patients with pulmonary fibrosis with mutations in the telomerase genes have a high rate of certain complications after lung transplantation. However, few studies have investigated clinical outcomes based on leukocyte telomere length. METHODS: We conducted an observational cohort study of all patients with pulmonary fibrosis who underwent lung transplantation at a single center between January 1, 2007, and December 31, 2014...
August 2017: Journal of Heart and Lung Transplantation
https://www.readbyqxmd.com/read/28254828/telomere-driven-diseases-and-telomere-targeting-therapies
#16
REVIEW
Paula Martínez, Maria A Blasco
Telomeres, the protective ends of linear chromosomes, shorten throughout an individual's lifetime. Telomere shortening is proposed to be a primary molecular cause of aging. Short telomeres block the proliferative capacity of stem cells, affecting their potential to regenerate tissues, and trigger the development of age-associated diseases. Mutations in telomere maintenance genes are associated with pathologies referred to as telomere syndromes, including Hoyeraal-Hreidarsson syndrome, dyskeratosis congenita, pulmonary fibrosis, aplastic anemia, and liver fibrosis...
April 3, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28192371/somatic-mutations-in-telomerase-promoter-counterbalance-germline-loss-of-function-mutations
#17
Lindley Maryoung, Yangbo Yue, Ashley Young, Chad A Newton, Cindy Barba, Nicolai S C van Oers, Richard C Wang, Christine Kim Garcia
Germline coding mutations in different telomere-related genes have been linked to autosomal-dominant familial pulmonary fibrosis. Individuals with these inherited mutations demonstrate incomplete penetrance of clinical phenotypes affecting the lung, blood, liver, skin, and other organs. Here, we describe the somatic acquisition of promoter mutations in telomerase reverse transcriptase (TERT) in blood leukocytes of approximately 5% of individuals with inherited loss-of-function coding mutations in TERT or poly(A)-specific ribonuclease (PARN), another gene linked to telomerase function...
March 1, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28154186/structural-analysis-reveals-the-deleterious-effects-of-telomerase-mutations-in-bone-marrow-failure-syndromes
#18
Hunter Hoffman, Cory Rice, Emmanuel Skordalakes
Naturally occurring mutations in the ribonucleoprotein reverse transcriptase, telomerase, are associated with the bone marrow failure syndromes dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis. However, the mechanism by which these mutations impact telomerase function remains unknown. Here we present the structure of the human telomerase C-terminal extension (or thumb domain) determined by the method of single-wavelength anomalous diffraction to 2.31 Å resolution. We also used direct telomerase activity and nucleic acid binding assays to explain how naturally occurring mutations within this portion of telomerase contribute to human disease...
March 17, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28145905/mitochondria-in-the-spotlight-of-aging-and-idiopathic-pulmonary-fibrosis
#19
REVIEW
Ana L Mora, Marta Bueno, Mauricio Rojas
Idiopathic pulmonary fibrosis (IPF) is a chronic age-related lung disease with high mortality that is characterized by abnormal scarring of the lung parenchyma. There has been a recent attempt to define the age-associated changes predisposing individuals to develop IPF. Age-related perturbations that are increasingly found in epithelial cells and fibroblasts from IPF lungs compared with age-matched cells from normal lungs include defective autophagy, telomere attrition, altered proteostasis, and cell senescence...
February 1, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28099038/an-exome-sequencing-study-to-assess-the-role-of-rare-genetic-variation-in-pulmonary-fibrosis
#20
Slavé Petrovski, Jamie L Todd, Michael T Durheim, Quanli Wang, Jason W Chien, Fran L Kelly, Courtney Frankel, Caroline M Mebane, Zhong Ren, Joshua Bridgers, Thomas J Urban, Colin D Malone, Ashley Finlen Copeland, Christie Brinkley, Andrew S Allen, Thomas O'Riordan, John G McHutchison, Scott M Palmer, David B Goldstein
RATIONALE: Idiopathic pulmonary fibrosis (IPF) is an increasingly recognized, often fatal lung disease of unknown etiology. OBJECTIVES: The aim of this study was to use whole-exome sequencing to improve understanding of the genetic architecture of pulmonary fibrosis. METHODS: We performed a case-control exome-wide collapsing analysis including 262 unrelated individuals with pulmonary fibrosis clinically classified as IPF according to American Thoracic Society/European Respiratory Society/Japanese Respiratory Society/Latin American Thoracic Association guidelines (81...
July 1, 2017: American Journal of Respiratory and Critical Care Medicine
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