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Hypothesis-generating for mutagenesis in atherosclerosis; leaves open antimutagen applications pending prospective trials.
Atherosclerosis causing by endothelial dysfunction following vascular inflammation can lead to thrombosis and artery occlusion, resulting in myocardial infarction, ischemic stroke, or peripheral artery disease. There is a convincing evidence on the impact of endogenous and exogenous mutagenesis in atherosclerosis; therefore, it can be partially considered as a neoplastic process. Here we describe the seminal papers in the field and provide the arguments on the association of mutagenesis with atherosclerosis. In particular, we underline the importance of oxidative stress, telomere dysfunction, DNA damage syndromes, and cytotoxic chemotherapy/radiotherapy. We also consider the therapeutical applications of antimutagens, particularly statins and angiotensin-converting enzyme inhibitors.
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Kutikhin et al. (2017) studied this question.
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