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

Harvard

Akbari, M, Shanley, DP, Bohr, VA & Rasmussen, LJ 2021, 'Cytosolic self-DNA—A potential source of chronic inflammation in aging', Cells, vol. 10, no. 12, 3544. https://doi.org/10.3390/cells10123544

APA

Akbari, M., Shanley, D. P., Bohr, V. A., & Rasmussen, L. J. (2021). Cytosolic self-DNA—A potential source of chronic inflammation in aging. Cells, 10(12), [3544]. https://doi.org/10.3390/cells10123544

Vancouver

Akbari M, Shanley DP, Bohr VA, Rasmussen LJ. Cytosolic self-DNA—A potential source of chronic inflammation in aging. Cells. 2021;10(12). 3544. https://doi.org/10.3390/cells10123544

Author

Akbari, Mansour ; Shanley, Daryl P. ; Bohr, Vilhelm A. ; Rasmussen, Lene Juel. / Cytosolic self-DNA—A potential source of chronic inflammation in aging. In: Cells. 2021 ; Vol. 10, No. 12.

Bibtex

@article{49f102a77e0b46109e90ed69106d385c,

title = "Cytosolic self-DNA—A potential source of chronic inflammation in aging",

abstract = "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.",

keywords = "Aging, CGAS-STING, Cytosolic self-DNA, DNA repair, Inflammation, Mitochondria",

author = "Mansour Akbari and Shanley, {Daryl P.} and Bohr, {Vilhelm A.} and Rasmussen, {Lene Juel}",

note = "Publisher Copyright: {\textcopyright} 2021 by the authors. Licensee MDPI, Basel, Switzerland.",

year = "2021",

doi = "10.3390/cells10123544",

language = "English",

volume = "10",

journal = "Cells",

issn = "2073-4409",

publisher = "MDPI AG",

number = "12",

}

RIS

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

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