Editing Atherosclerosis (section)

===DNA damage===
[[Aging]] is the most important risk factor for cardiovascular problems.  The causative basis by which aging mediates its impact, independently of other recognized risk factors, remains to be determined.  Evidence has been reviewed for a key role of [[DNA damage (naturally occurring)|DNA damage]] in vascular aging.<ref name="pmid23953979">{{cite journal | vauthors = Wu H, Roks AJ | title = Genomic instability and vascular aging: a focus on nucleotide excision repair | journal = Trends in Cardiovascular Medicine | volume = 24 | issue = 2 | pages = 61–68 | date = February 2014 | pmid = 23953979 | doi = 10.1016/j.tcm.2013.06.005 }}</ref><ref name="pmid27213333">{{cite journal | vauthors = Bautista-Niño PK, Portilla-Fernandez E, Vaughan DE, Danser AH, Roks AJ | title = DNA Damage: A Main Determinant of Vascular Aging | journal = International Journal of Molecular Sciences | volume = 17 | issue = 5 | page = 748 | date = May 2016 | pmid = 27213333 | pmc = 4881569 | doi = 10.3390/ijms17050748 | doi-access = free }}</ref><ref name="pmid28347738">{{cite journal | vauthors = Shah AV, Bennett MR | title = DNA damage-dependent mechanisms of ageing and disease in the macro- and microvasculature | journal = European Journal of Pharmacology | volume = 816 | pages = 116–128 | date = December 2017 | pmid = 28347738 | doi = 10.1016/j.ejphar.2017.03.050 | url = https://www.repository.cam.ac.uk/handle/1810/264776 }}</ref>
[[8-Oxoguanine|8-oxoG]], a common type of oxidative damage in [[DNA]], is found to accumulate in plaque [[vascular smooth muscle]] cells, [[macrophage]]s and [[endothelium|endothelial cells]],<ref name="pmid12186795">{{cite journal | vauthors = Martinet W, Knaapen MW, De Meyer GR, Herman AG, Kockx MM | title = Elevated levels of oxidative DNA damage and DNA repair enzymes in human atherosclerotic plaques | journal = Circulation | volume = 106 | issue = 8 | pages = 927–932 | date = August 2002 | pmid = 12186795 | doi = 10.1161/01.cir.0000026393.47805.21 | doi-access = free }}</ref> thus linking DNA damage to plaque formation. DNA strand breaks also increased in atherosclerotic plaques.<ref name="pmid12186795" />  [[Werner syndrome]] (WS) is a premature aging condition in humans.<ref name="pmid24334614">{{cite journal | vauthors = Ishida T, Ishida M, Tashiro S, Yoshizumi M, Kihara Y | title = Role of DNA damage in cardiovascular disease | journal = Circulation Journal | volume = 78 | issue = 1 | pages = 42–50 | year = 2014 | pmid = 24334614 | doi = 10.1253/circj.CJ-13-1194 | doi-access = free }}</ref>  WS is caused by a genetic defect in a [[RecQ helicase]] that is employed in several [[DNA repair|repair processes that remove damages from DNA]].  WS patients develop a considerable burden of atherosclerotic plaques in their [[Coronary circulation|coronary arteries]] and [[aorta]]: calcification of the aortic valve is also frequently observed.<ref name="pmid27213333" />  These findings link excessive unrepaired DNA damage to premature aging and early atherosclerotic plaque development (see [[DNA damage theory of aging]]).{{citation needed|date=December 2020}}