Highlights
- •Accumulating evidence indicates that genomic instability triggers inflammation.
- •Cellular senescence is involved in the mechanisms of inflammation through senescence-associated secretory phenotype.
- •Not only the microbial DNA but also the fragmented self-DNA in the cytosol can trigger inflammation.
- •Recognition of fragmented DNA in the cytosol by DNA sensors induces intracellular processes that lead to inflammation.
Abstract
Atherosclerosis is a cause of coronary artery disease, abdominal aortic aneurysm,
and stroke. The pathogenesis underlying atherosclerosis is complex but it is clear
that inflammation plays a pivotal role. Inflammation in atherosclerosis is triggered
by the recognition of intracellular contents released from damaged cells by pattern
recognition receptors, and is therefore sterile and chronic. Because the DNA of these
cells is damaged, cellular senescence is also involved in this inflammation. Here,
we will discuss the emerging evidence of a relationship between DNA damage and inflammation
in the pathogenesis of atherosclerosis, with a focus on intracellular events and cell
fates that arise following DNA damage. Recent evidence will lead us to potential therapeutic
targets and allow us to explore potential preventative and therapeutic strategies.
Graphical abstract
Graphical Abstract
Keywords
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Article info
Publication history
Published online: September 12, 2022
Accepted:
August 21,
2022
Received:
August 10,
2022
Identification
Copyright
© 2022 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved. All rights reserved.
