TNFA gene variants related to the inflammatory status and its association with cellular aging: From the CORDIOPREV study

[1]  J. Muñóz-Valle,et al.  Association of the -1031T>C polymorphism and soluble TNF-α levels with Acute Coronary Syndrome. , 2016, Cytokine.

[2]  C. Tovilla-Zárate,et al.  The role of gene variants of the inflammatory markers CRP and TNF-α in cardiovascular heart disease: systematic review and meta-analysis. , 2015, International journal of clinical and experimental medicine.

[3]  J. Vijg,et al.  Genetic evidence for common pathways in human age-related diseases , 2015, Aging cell.

[4]  F. Tinahones,et al.  Influence of endothelial dysfunction on telomere length in subjects with metabolic syndrome: LIPGENE study , 2014, AGE.

[5]  J. Ordovás,et al.  Polymorphism at the TNF-alpha gene interacts with Mediterranean diet to influence triglyceride metabolism and inflammation status in metabolic syndrome patients: From the CORDIOPREV clinical trial. , 2014, Molecular nutrition & food research.

[6]  Arjun K. Ghosh,et al.  Rate of telomere shortening and cardiovascular damage: a longitudinal study in the 1946 British Birth Cohort , 2014, European heart journal.

[7]  Eric E Schadt,et al.  The role of macromolecular damage in aging and age-related disease. , 2014, The journals of gerontology. Series A, Biological sciences and medical sciences.

[8]  Clara Correia-Melo,et al.  Telomeres, oxidative stress and inflammatory factors: partners in cellular senescence? , 2014, Longevity & healthspan.

[9]  Manuel Serrano,et al.  The Hallmarks of Aging , 2013, Cell.

[10]  M. Armanios Telomeres and age-related disease: how telomere biology informs clinical paradigms. , 2013, The Journal of clinical investigation.

[11]  A. Chuturgoon,et al.  Telomeres and atherosclerosis , 2012, Cardiovascular journal of Africa.

[12]  R. Hui,et al.  Polymorphism of tumor necrosis factor alpha (TNF-alpha) gene promoter, circulating TNF-alpha level, and cardiovascular risk factor for ischemic stroke , 2012, Journal of Neuroinflammation.

[13]  N. R. Jena DNA damage by reactive species: Mechanisms, mutation and repair , 2012, Journal of Biosciences.

[14]  M. Malagón,et al.  Dietary fat modifies the postprandial inflammatory state in subjects with metabolic syndrome: the LIPGENE study. , 2012, Molecular nutrition & food research.

[15]  Jun Yang,et al.  Tumor necrosis factor-alpha G-308 A polymorphism and risk of coronary heart disease and myocardial infarction: A case-control study and meta-analysis , 2012, Journal of cardiovascular disease research.

[16]  Claudio J. Verzilli,et al.  Comparative analysis of genome-wide association studies signals for lipids, diabetes, and coronary heart disease: Cardiovascular Biomarker Genetics Collaboration , 2011, European heart journal.

[17]  Roberto Sacco,et al.  Age- and gender-specific epistasis between ADA and TNF-α influences human life-expectancy. , 2011, Cytokine.

[18]  R. Pandey,et al.  Associations of −308G/A Polymorphism of Tumor Necrosis Factor(TNF)–α Gene and Serum TNF-α Levels with Measures of Obesity, Intra-Abdominal and Subcutaneous Abdominal Fat, Subclinical Inflammation and Insulin Resistance in Asian Indians in North India , 2011, Disease markers.

[19]  Javier Martín,et al.  TNFA -308 (rs1800629) polymorphism is associated with a higher risk of cardiovascular disease in patients with rheumatoid arthritis. , 2011, Atherosclerosis.

[20]  H. Ostrer,et al.  The History of African Gene Flow into Southern Europeans, Levantines, and Jews , 2011, PLoS genetics.

[21]  G. Navis,et al.  LPL polymorphism (D9N) predicts cardiovascular disease risk directly and through interaction with CETP polymorphism (TaqIB) in women with high HDL cholesterol and CRP. , 2011, Atherosclerosis.

[22]  Michael J Morgan,et al.  Crosstalk of reactive oxygen species and NF-κB signaling , 2011, Cell Research.

[23]  N. Zhang,et al.  Inflammation and reactive oxygen species in cardiovascular disease. , 2010, World journal of cardiology.

[24]  L. Cupples,et al.  Additive effect of polymorphisms in the IL-6, LTA, and TNF-{alpha} genes and plasma fatty acid level modulate risk for the metabolic syndrome and its components. , 2010, The Journal of clinical endocrinology and metabolism.

[25]  Z. Ďuračková Some current insights into oxidative stress. , 2010, Physiological research.

[26]  R. Weinberg,et al.  Continuous elimination of oxidized nucleotides is necessary to prevent rapid onset of cellular senescence , 2009, Proceedings of the National Academy of Sciences.

[27]  Judith Campisi,et al.  Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor , 2008, PLoS biology.

[28]  T. Finkel,et al.  Free radicals and senescence. , 2008, Experimental cell research.

[29]  C. Franceschi,et al.  A genetic-demographic approach reveals male-specific association between survival and tumor necrosis factor (A/G)-308 polymorphism. , 2008, The journals of gerontology. Series A, Biological sciences and medical sciences.

[30]  M. Blasco,et al.  Cellular Senescence in Cancer and Aging , 2007, Cell.

[31]  G. Mellick TNF Polymorphism and Cardiovascular Disease: TNF gene polymorphism and quantitative traits related to cardiovascular disease: getting to the heart of the matter , 2007, European Journal of Human Genetics.

[32]  C. Caruso,et al.  Inflammatory networks in ageing, age-related diseases and longevity , 2007, Mechanisms of Ageing and Development.

[33]  C. Falcone,et al.  Inflammation and Atherosclerosis: The Role of TNF and TNF Receptors Polymorphisms in Coronary Artery Disease , 2007, International journal of immunopathology and pharmacology.

[34]  G. Lucotte,et al.  North African Berber and Arab Influences in the Western Mediterranean Revealed by Y-Chromosome DNA Haplotypes , 2006, Human biology.

[35]  C. Iadecola,et al.  NF-κB Regulates Phagocytic NADPH Oxidase by Inducing the Expression of gp91phox* , 2006, Journal of Biological Chemistry.

[36]  T. Zglinicki Role of oxidative stress in telomere length regulation and replicative senescence , 2006 .

[37]  D. Kurz,et al.  Cellular senescence in vivo: Its relevance in ageing and cardiovascular disease , 2005, Experimental Gerontology.

[38]  G. O’Keefe,et al.  Defining the proinflammatory phenotype using high sensitive C-reactive protein levels as the biomarker. , 2005, The Journal of clinical endocrinology and metabolism.

[39]  R. Colavitti,et al.  Reactive Oxygen Species as Mediators of Cellular Senescence , 2005, IUBMB life.

[40]  L. Bautista,et al.  Independent association between inflammatory markers (C-reactive protein, interleukin-6, and TNF-α) and essential hypertension , 2005, Journal of Human Hypertension.

[41]  Mark Daly,et al.  Haploview: analysis and visualization of LD and haplotype maps , 2005, Bioinform..

[42]  L. Sabatier,et al.  Tumor necrosis factor alpha induces senescence and chromosomal instability in human leukemic cells , 2004, Oncogene.

[43]  A. Ceriello,et al.  Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease? The common soil hypothesis revisited. , 2004, Arteriosclerosis, thrombosis, and vascular biology.

[44]  M. Pfaffl,et al.  Determination of stable housekeeping genes, differentially regulated target genes and sample integrity: BestKeeper – Excel-based tool using pair-wise correlations , 2004, Biotechnology Letters.

[45]  C. Franceschi,et al.  Inflammation, genetics, and longevity: further studies on the protective effects in men of IL-10 −1082 promoter SNP and its interaction with TNF-α −308 promoter SNP , 2003, Journal of medical genetics.

[46]  T. Zglinicki Oxidative stress shortens telomeres , 2002 .

[47]  R. Cawthon Telomere measurement by quantitative PCR. , 2002, Nucleic acids research.

[48]  G. Saretzki,et al.  BJ fibroblasts display high antioxidant capacity and slow telomere shortening independent of hTERT transfection. , 2001, Free radical biology & medicine.

[49]  Zhongmao Guo,et al.  Does oxidative damage to DNA increase with age? , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[50]  J. de Magalhães,et al.  Growth kinetics rather than stress accelerate telomere shortening in cultures of human diploid fibroblasts in oxidative stress‐induced premature senescence , 2001, FEBS letters.

[51]  S. Oikawa,et al.  Site-specific DNA damage at the GGG sequence by UVA involves acceleration of telomere shortening. , 2001, Biochemistry.

[52]  G. Thomas,et al.  Asp-Ala-His-Lys (DAHK) inhibits copper-induced oxidative DNA double strand breaks and telomere shortening. , 2001, Biochemical and biophysical research communications.

[53]  T. Zglinicki,et al.  Accumulation of single-strand breaks is the major cause of telomere shortening in human fibroblasts. , 2000, Free radical biology & medicine.

[54]  S. Petersen,et al.  Preferential accumulation of single-stranded regions in telomeres of human fibroblasts. , 1998, Experimental cell research.

[55]  T. Davison,et al.  ATM‐dependent telomere loss in aging human diploid fibroblasts and DNA damage lead to the post‐translational activation of p53 protein involving poly(ADP‐ribose) polymerase , 1997, The EMBO journal.

[56]  Shirley A. Miller,et al.  A simple salting out procedure for extracting DNA from human nucleated cells. , 1988, Nucleic acids research.