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. / Akbari, Mansour; Shanley, Daryl P.; Bohr, Vilhelm A.; Rasmussen, Lene Juel.
In: Cells, Vol. 10, No. 12, 3544, 2021.Research output: Contribution to journal › Review › Research › peer-review
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TY - JOUR
T1 - Cytosolic self-DNA—A potential source of chronic inflammation in aging
AU - Akbari, Mansour
AU - Shanley, Daryl P.
AU - Bohr, Vilhelm A.
AU - Rasmussen, Lene Juel
N1 - Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021
Y1 - 2021
N2 - 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.
AB - 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.
KW - Aging
KW - CGAS-STING
KW - Cytosolic self-DNA
KW - DNA repair
KW - Inflammation
KW - Mitochondria
U2 - 10.3390/cells10123544
DO - 10.3390/cells10123544
M3 - Review
C2 - 34944052
AN - SCOPUS:85121097603
VL - 10
JO - Cells
JF - Cells
SN - 2073-4409
IS - 12
M1 - 3544
ER -
ID: 287701118