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Updated: Aug 28, 2025
Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
Published on: August 21, 2021
Role of DNA damage in the pathogenesis of atherosclerosis
Mari Ishida1, Chiemi Sakai1, Takafumi Ishida2
1Department of Cardiovascular Physiology and Medicine, Hiroshima University, Hiroshima, Japan.
Insights
DNA damage triggers sterile inflammation in atherosclerosis, a complex disease causing heart attack and stroke. Understanding this link reveals new therapeutic targets for prevention and treatment.
Area of Science:
- Cardiovascular Science
- Inflammation Research
- Molecular Biology
Background:
- Atherosclerosis is a major cause of cardiovascular diseases, including coronary artery disease, abdominal aortic aneurysm, and stroke.
- Inflammation is a critical factor in atherosclerosis pathogenesis, often initiated by intracellular components from damaged cells.
- Cellular senescence, linked to DNA damage, also contributes to chronic inflammation in atherosclerosis.
Purpose of the Study:
- To explore the relationship between DNA damage and inflammation in atherosclerosis.
- To focus on intracellular events and cell fates following DNA damage in atherosclerosis.
- To identify potential therapeutic targets and strategies for atherosclerosis.
Main Methods:
- Review of emerging scientific evidence.
- Analysis of intracellular events and cell fates.
- Discussion of potential therapeutic interventions.
Main Results:
- DNA damage is a key initiator of sterile, chronic inflammation in atherosclerosis.
- Cellular senescence is implicated in the inflammatory processes of atherosclerosis.
- The interplay between DNA damage and inflammation offers promising avenues for therapeutic development.
Conclusions:
- Targeting the DNA damage-inflammation axis presents a novel strategy for atherosclerosis treatment.
- Further research into intracellular events post-DNA damage can guide preventative and therapeutic approaches.
- Understanding cellular senescence in atherosclerosis may unlock new treatment possibilities.
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.
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