Journal article : Review
DNA damage response, a double-edged sword for vascular aging
- Abstract:
- Vascular aging is a major risk factor for age-related cardiovascular diseases, which have high rates of morbidity and mortality. It is characterized by changes in the blood vessels, such as macroscopically increased vascular diameter and intima-medial thickness, chronic inflammation, vascular calcification, arterial stiffening, and atherosclerosis. DNA damage and the subsequent various DNA damage response (DDR) pathways are important causative factors of vascular aging. Deficient DDR, which may result in the accumulation of unrepaired damaged DNA or mutations, can lead to vascular aging. On the other hand, over-activation of some DDR proteins, such as poly (ADP ribose) polymerase (PARP) and ataxia telangiectasia mutated (ATM), also can enhance the process of vascular aging, suggesting that DDR can have both positive and negative effects on vascular aging. Despite the evidence reviewed in this paper, the role of DDR in vascular aging and potential therapeutic targets remain poorly understood and require further investigation.
- Publication status:
- Published
- Peer review status:
- Peer reviewed
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(Preview, Version of record, pdf, 3.7MB, Terms of use)
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- Publisher copy:
- 10.1016/j.arr.2023.102137
Authors
+ Cancer Research UK
More from this funder
- Funder identifier:
- https://ror.org/054225q67
- Grant:
- 24866
- Publisher:
- Elsevier
- Journal:
- Ageing Research Reviews More from this journal
- Volume:
- 92
- Article number:
- 102137
- Publication date:
- 2023-11-23
- Acceptance date:
- 2023-11-20
- DOI:
- EISSN:
-
1872-9649
- ISSN:
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1568-1637
- Pmid:
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38007046
- Language:
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English
- Keywords:
- Subtype:
-
Review
- Pubs id:
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1570749
- Local pid:
-
pubs:1570749
- Deposit date:
-
2025-02-03
Terms of use
- Copyright holder:
- Zhang et al.
- Copyright date:
- 2023
- Rights statement:
- © 2023 The Author(s). Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
- Licence:
- CC Attribution (CC BY)
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