TNFA gene variants related to the inflammatory status and its association with cellular aging: From the CORDIOPREV study
Abstract
Background Several single nucleotide polymorphisms have been proposed as potential predictors of the development of age-related diseases.Objective To explore whether Tumor Necrosis Factor Alpha (TNFA) gene variants were associated with inflammatory status, thus facilitating the rate of telomere shortening and its relation to cellular aging in a population with established cardiovascular disease from the CORDIOPREV study (NCT00924937).Materials and methods SNPs (rs1800629 and rs1799964) located at the TNFA gene were genotyped by OpenArray platform in 840 subjects with established cardiovascular disease. Relative telomere length was determined by real time PCR and plasma levels of C-reactive protein by ELISA. In a subgroup of 90 subjects, the gene expression profiles of TNFA, IKKβ, p47phox, p40phox, p22phox and gp91phox were determined by qRT-PCR.Results GG subjects for the SNP rs1800629 at the TNFA gene showed shorter relative telomere length and higher plasma levels of hs-CRP than A-allele subjects (p<0.05). Consistent with these findings, the expression of pro-inflammatory (TNFA) and pro-oxidant (p47phox and the gp91phox) genes was higher in GG subjects than A allele subjects (p<0.05).Conclusion Subjects carrying the GG genotype for the SNP rs1800629 at the TNFA gene show a greater activation of the proinflammatory status than A-allele carriers, which is related to ROS formation. These ROS could induce DNA damage especially in the telomeric sequence, by decreasing the telomere length and inducing cellular aging. This effect may also increase the risk of the development of age-related diseases.
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Increased oxidative stress is a major driver of senescence.
“Increased oxidative stress (OS) is a further major driver of senescence [16,17,18,19,20,21].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [20]
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- Authors
- Rangel-Zúñiga, O. A., Corina, A., Lucena-Porras, B., Cruz-Teno, C., Gómez-Delgado, F., Jiménez-Lucena, R., Alcalá-Díaz, J. F., Haro-Mariscal, C., Yubero-Serrano, E. M., Delgado-Lista, J., López-Moreno, J., Rodríguez-Cantalejo, F., Camargo, A., Tinahones, F. J., Ordovás, J. M., López-Miranda, J., & Pérez-Martínez, P.
- Affiliations
- Instituto de Salud Carlos III (ES)
- Hospital Universitario Reina Sofía (ES)
- Madrid Institute for Advanced Studies (ES)
- ORCID
- Venue
- Experimental Gerontology
- Publisher
- Elsevier BV
- Published
- 2016-10
- Volume
- 83
- Pages
- 56-62
- ISSN
- 0531-5565 (ISSN-L)
- OpenAlex
- W2502780453
- Cited by
- 11
- References
- 57
- Citations by year
- 2022: 2 · 2020: 1 · 2019: 5 · 2018: 3
- FWCI
- 2.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental Gerontology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministerio de Economía y Competitividad (FIS PI13/00185, AGL2012/39615)
- Proyecto de Excelencia, Consejería de Economía, Innovación, Ciencia y Empleo (CVI-7450)
- European Community (289511)
- Fondo Europeo de Desarrollo Regional (FEDER)
- ISCIII (CP14/00114)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- TNF-α, rs1800629, rs1799964, telomere length, cellular aging, inflammation, C-reactive protein, oxidative stress, NADPH oxidase, gp91phox, p47phox, p40phox, p22phox, IKKβ, age-related diseases, cardiovascular disease, DNA damage
- MeSH terms
- Aged, Alleles, C-Reactive Protein, Female, Humans, Inflammation, Male, Spain, Tumor Necrosis Factor-alpha, Gene Expression, Randomized Controlled Trials as Topic, Telomere, Cellular Senescence, Reactive Oxygen Species, Oxidative Stress, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Telomere Shortening
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