Telomeres as hotspots for innate immunity and inflammation
Aging is marked by the gradual accumulation of deleterious changes that disrupt organ function, creating an altered physiological state that is permissive for the onset of prevalent human diseases. While the exact mechanisms governing aging remain a subject of ongoing research, there are several cel...
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Published in | DNA repair Vol. 133; p. 103591 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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01.01.2024
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Abstract | Aging is marked by the gradual accumulation of deleterious changes that disrupt organ function, creating an altered physiological state that is permissive for the onset of prevalent human diseases. While the exact mechanisms governing aging remain a subject of ongoing research, there are several cellular and molecular hallmarks that contribute to this biological process. This review focuses on two factors, namely telomere dysfunction and inflammation, which have emerged as crucial contributors to the aging process. We aim to discuss the mechanistic connections between these two distinct hallmarks and provide compelling evidence highlighting the loss of telomere protection as a driver of pro-inflammatory states associated with aging. By reevaluating the interplay between telomeres, innate immunity, and inflammation, we present novel perspectives on the etiology of aging and its associated diseases. |
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AbstractList | Aging is marked by the gradual accumulation of deleterious changes that disrupt organ function, creating an altered physiological state that is permissive for the onset of prevalent human diseases. While the exact mechanisms governing aging remain a subject of ongoing research, there are several cellular and molecular hallmarks that contribute to this biological process. This review focuses on two factors, namely telomere dysfunction and inflammation, which have emerged as crucial contributors to the aging process. We aim to discuss the mechanistic connections between these two distinct hallmarks and provide compelling evidence highlighting the loss of telomere protection as a driver of pro-inflammatory states associated with aging. By reevaluating the interplay between telomeres, innate immunity, and inflammation, we present novel perspectives on the etiology of aging and its associated diseases.Aging is marked by the gradual accumulation of deleterious changes that disrupt organ function, creating an altered physiological state that is permissive for the onset of prevalent human diseases. While the exact mechanisms governing aging remain a subject of ongoing research, there are several cellular and molecular hallmarks that contribute to this biological process. This review focuses on two factors, namely telomere dysfunction and inflammation, which have emerged as crucial contributors to the aging process. We aim to discuss the mechanistic connections between these two distinct hallmarks and provide compelling evidence highlighting the loss of telomere protection as a driver of pro-inflammatory states associated with aging. By reevaluating the interplay between telomeres, innate immunity, and inflammation, we present novel perspectives on the etiology of aging and its associated diseases. Aging is marked by the gradual accumulation of deleterious changes that disrupt organ function, creating an altered physiological state that is permissive for the onset of prevalent human diseases. While the exact mechanisms governing aging remain a subject of ongoing research, there are several cellular and molecular hallmarks that contribute to this biological process. This review focuses on two factors, namely telomere dysfunction and inflammation, which have emerged as crucial contributors to the aging process. We aim to discuss the mechanistic connections between these two distinct hallmarks and provide compelling evidence highlighting the loss of telomere protection as a driver of pro-inflammatory states associated with aging. By reevaluating the interplay between telomeres, innate immunity, and inflammation, we present novel perspectives on the etiology of aging and its associated diseases. |
ArticleNumber | 103591 |
Author | Nassour, Joe Przetocka, Sara Karlseder, Jan |
AuthorAffiliation | b The Salk Institute for Biological Studies, 10010 North Torrey Pines Rd, La Jolla, CA 92037, USA a Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, 12801 E. 17th Ave, Aurora, CO 80045, USA |
AuthorAffiliation_xml | – name: a Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, 12801 E. 17th Ave, Aurora, CO 80045, USA – name: b The Salk Institute for Biological Studies, 10010 North Torrey Pines Rd, La Jolla, CA 92037, USA |
Author_xml | – sequence: 1 givenname: Joe surname: Nassour fullname: Nassour, Joe – sequence: 2 givenname: Sara surname: Przetocka fullname: Przetocka, Sara – sequence: 3 givenname: Jan orcidid: 0000-0001-7433-9750 surname: Karlseder fullname: Karlseder, Jan |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37951043$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1093_neuonc_noae016 crossref_primary_10_3389_fimmu_2024_1465006 crossref_primary_10_1038_s41580_024_00800_5 |
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Keywords | Aging Telomeres Innate immunity Inflammation Genome stability Cancer |
Language | English |
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