The DOI matches its Crossref record; 148 of the 148 references it cites were found in a registry or an index.
Telomeres and immunological diseases of aging.
Open accessAbstract
A defining feature of the eukaryotic genome is the presence of linear chromosomes. This arrangement, however, poses several challenges with regard to chromosomal replication and maintenance. To prevent the loss of coding sequences and to suppress gross chromosomal rearrangements, linear chromosomes are capped by repetitive nucleoprotein structures, called telomeres. Each cell division results in a progressive shortening of telomeres that, below a certain threshold, promotes genome instability, senescence, and apoptosis. Telomeric erosion, maintenance, and repair take center stage in determining cell fate. Cells of the immune system are under enormous proliferative demand, stressing telomeric intactness. Lymphocytes are capable of upregulating telomerase, an enzyme that can elongate telomeric sequences and, thus, prolong cellular lifespan. Therefore, telomere dynamics are critical in preserving immune function and have become a focus for studies of immunosenescence and autoimmunity. In this review, we describe the role of telomeric nucleoproteins in shaping telomere architecture and in suppressing DNA damage responses. We summarize new insights into the regulation of telomerase activity, hereditary disorders associated with telomere dysfunction, the role of telomere loss in immune aging, and the impact of telomere dysfunction in chronic inflammatory disease.
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“In contrast to most other somatic cells, they have the ability to reactivate telomerase, elongate telomeres and thus lengthen their life span [13].”
From T-cell aging in rheumatoid arthritis (2014) · cites this paper as [13]
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“HIV-associated inflammation and/or exposure to nucleoside analogues have been associated with changes in these and other key biologic pathways (33–40).”
From HIV and Aging: State of Knowledge and Areas of Critical Need for Research. A Report to the NIH Office of AIDS Research by the HIV and Aging Working Group (2012) · cites this paper as [37]
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1 retracted
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RetractedThe serial cultivation of human diploid cell strains
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“Regulation of Telomerase ActivityIn the process of carcinogenesis, cells escape senescence through the mutation of tumor suppressor genes and survive crisis through telomerase upregulation. Thus, approximately 90p of tumor cells are positive for telomerase activity [”
BackgroundShelterin: the protein complex that shapes and safeguards human telomeres
de Lange, T. (2005) · Genes & Development · doi:10.1101/gad.1346005 · Cited by 3,056
Oxidative stress shortens telomeres
von Zglinicki, T. (2002) · Trends in Biochemical Sciences · doi:10.1016/s0968-0004(02)02110-2 · Cited by 2,524
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Research works printed but not linked: 2
- 10.1016%2FS0092-8674%2803%2900550-6 · DOI · Paper page
- 10.1203%2F01.PDR.0000022341.72856.72 · DOI
Cited by
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Understanding immunosenescence to improve responses to vaccines
Goronzy, J. J., & Weyand, C. M. (2013) · Nature Immunology · doi:10.1038/ni.2588 · Cited by 827
Self-citationAging of the Immune System. Mechanisms and Therapeutic Targets
Weyand, C. M., & Goronzy, J. J. (2016) · Annals of the American Thoracic Society · doi:10.1513/annalsats.201602-095aw · Cited by 586
Self-citationThe risk of infections associated with rheumatoid arthritis, with its comorbidity and treatment
Listing, J., Gerhold, K., & Zink, A. (2013) · Rheumatology · doi:10.1093/rheumatology/kes305 · Cited by 541
High, K. P., Brennan-Ing, M., Clifford, D. B., Cohen, M. H., Currier, J., Deeks, S. G., Deren, S., Effros, R. B., Gebo, K., Goronzy, J. J., et al. (2012) · JAIDS Journal of Acquired Immune Deficiency Syndromes · doi:10.1097/qai.0b013e31825a3668 · Cited by 522
Self-citationAgeing and the telomere connection: An intimate relationship with inflammation
Zhang, J., Rane, G., Dai, X., Shanmugam, M. K., Arfuso, F., Samy, R. P., Lai, M. K. P., Kappei, D., Kumar, A. P., & Sethi, G. (2015) · Ageing Research Reviews · doi:10.1016/j.arr.2015.11.006 · Cited by 396
Metadata
- Authors
- Andrews, N. P., Fujii, H., Goronzy, J. J., & Weyand, C. M.
- Affiliations
- Emory University (US)
- Venue
- Gerontology
- Publisher
- S. Karger AG
- Published
- 2009-12-17
- Volume
- 56
- Issue
- 4
- Pages
- 390-403
- ISSN
- 0304-324X (ISSN-L)
- 1423-0003
- PMC
- PMC2917738
- OpenAlex
- W1981392889
- Cited by
- 108
- References
- 148
- Citations by year
- 2025: 3 · 2024: 12 · 2023: 4 · 2022: 5 · 2021: 5 · 2020: 5 · 2019: 5 · 2018: 9 · 2017: 2 · 2016: 5 · 2015: 7 · 2014: 12 · 2013: 8 · 2012: 15
- FWCI
- 0.91
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Gerontology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American College of Rheumatology Research and Education Foundation
- Rheumatology Research Foundation
- National Institutes of Health
- National Institute on Aging (R01AG015043, R01AG15043)
- National Heart, Lung, and Blood Institute (R01HL117913)
- National Eye Institute (R01EY011916, R01 EY 11916)
- National Institute of Allergy and Infectious Diseases (R01AI044142, U19-AI57266, R01AI44142, R01AI108906, R56AI044142, U19AI057266)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR041974, R01 AR 41974, R01AR042527, R01AR42527)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Keywords
- telomeres, immunosenescence, autoimmunity, telomerase, telomere dysfunction, lymphocytes, telomere maintenance, DNA damage response, chronic inflammatory diseases, genomic instability, cellular senescence, apoptosis
- MeSH terms
- Aging, Animals, Humans, Immune System Diseases, Inflammation, Models, Biological, T-Lymphocytes, Gene Expression Regulation, Enzymologic, Telomere, Cellular Senescence, Telomerase, Aging, Premature
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