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Chapter 10. DNA Damage Responses in Atherosclerosis
出版Elsevier Inc. Chapters, 2013-10-30
主題Medical / ImmunologyScience / Life Sciences / Microbiology
ISBN01280688339780128068830
URLhttp://books.google.com.hk/books?id=-odzDAAAQBAJ&hl=&source=gbs_api
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註釋DNA damage exists in all cellular organisms. While DNA damage is distinguished from mutation, mutation can result from unrepaired DNA. While most DNA damage can be repaired, such repair systems are not 100% efficient. Un-repaired DNA damage accumulates in non-replicating cells, such as neurons or myocytes of adult mammals, and can cause aging. DNA damage can be subdivided into two types: (1) endogenous damage caused by reactive oxygen species (ROS) that are derived from metabolic byproducts and (2) exogenous damage caused by radiation (UV, X-ray, gamma), hydrolysis, plant toxins, and viruses. Current data suggest that increased oxidative stress is a major characteristic of hypercholesterolemia-induced atherosclerosis and that oxidative stress is most likely associated with DNA damage in the development of cholesterol-induced plaques. This chapter critically addresses the extent to which the DNA damage, the sensing of it, and DNA damage repair are involved in the pathogenesis of atherosclerosis.