- 作者: Paolo Puddu; Giovanni M Puddu; Eleonora Cravero; Susanna De Pascalis; Antonio Muscari
- 作者服務機構: Department of Internal Medicine, Aging and Nephrological Diseases, University of Bologna and S. Orsola-Malpighi Hospital, Bologna, Italy
- 中文摘要: --
- 英文摘要:
An important role in atherogenesis is played by oxidative stress, which may be induced by common
risk factors. Mitochondria are both sources and targets of reactive oxygen species, and there is
growing evidence that mitochondrial dysfunction may be a relevant intermediate mechanism by which
cardiovascular risk factors lead to the formation of vascular lesions. Mitochondrial DNA is probably
the most sensitive cellular target of reactive oxygen species. Damage to mitochondrial DNA correlates
with the extent of atherosclerosis. Several cardiovascular risk factors are demonstrated causes of
mitochondrial damage. Oxidized low density lipoprotein and hyperglycemia may induce the
production of reactive oxygen species in mitochondria of macrophages and endothelial cells.
Conversely, reactive oxygen species may favor the development of type 2 diabetes mellitus, mainly
through the induction of insulin resistance. Similarly - in addition to being a cause of endothelial
dysfunction, reactive oxygen species and subsequent mitochondrial dysfunction - hypertension may
develop in the presence of mitochondrial DNA mutations. Finally, other risk factors, such as aging,
hyperhomocysteinemia and cigarette smoking, are also associated with mitochondrial damage and an
increased production of free radicals. So far clinical studies have been unable to demonstrate that
antioxidants have any effect on human atherogenesis. Mitochondrial targeted antioxidants might
provide more significant results. - 中文關鍵字: --
- 英文關鍵字: --