Cytosolic self-DNA—A potential source of chronic inflammation in aging
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- Cytosolic Self-DNA—A Potential Source of Chronic Inflammation in Aging
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Aging is the consequence of a lifelong accumulation of stochastic damage to tissues and cellular components. Advancing age closely associates with elevated markers of innate immunity and low-grade chronic inflammation, probably reflecting steady increasing incidents of cellular and tissue damage over the life course. The DNA sensing cGAS-STING signaling pathway is activated by misplaced cytosolic self-DNA, which then initiates the innate immune responses. Here, we hypothesize that the stochastic release of various forms of DNA from the nucleus and mitochondria, e.g., because of DNA damage, altered nucleus integrity, and mitochondrial damage, can result in chronic activation of inflammatory responses that characterize the aging process. This cytosolic self-DNA-innate immunity axis may perturb tissue homeostasis and function that characterizes human aging and age-associated pathology. Proper techniques and experimental models are available to investigate this axis to develop therapeutic interventions.
Originalsprog | Engelsk |
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Artikelnummer | 3544 |
Tidsskrift | Cells |
Vol/bind | 10 |
Udgave nummer | 12 |
ISSN | 2073-4409 |
DOI | |
Status | Udgivet - 2021 |
Bibliografisk note
Funding Information:
Author Contributions: Conceptualization, M.A. and L.J.R.; writing—original draft preparation, M.A.; writing—review and editing, M.A., D.P.S., V.A.B., L.J.R. All authors have read and agreed to the published version of the manuscript Funding: This works was supported by Nordea-fonden, Denmark (02-2013-0220); Novo Nordisk foundation Denmark (NNF17OC0027812); and Intramural Research Program of the NIH, National Institute on Aging (AG000733). LJR is a member of the Clinical Academic Group: Recovery Capacity After Acute Illness in An Aging Population (RECAP).
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© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
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