氧化应激
线粒体
活性氧
自噬
糖尿病
2型糖尿病
氧化磷酸化
抗氧化剂
线粒体ROS
维生素E
细胞生物学
生物
化学
医学
内分泌学
内科学
生物化学
细胞凋亡
作者
Víctor M. Víctor,Milagros Rocha,José Raúl Herance,Antonio Hernández‐Mijares
标识
DOI:10.2174/138161211798764915
摘要
Diabetes is a chronic disease and, as a consequence of the overproduction of reactive oxygen species (ROS), is related with oxidative stress. There are different sources of ROS, of which mitochondria is the main one. Oxidative stress seems to play an important role in mitochondria- mediated disease processes, though the exact molecular mechanisms responsible remain elusive. There are evidences which supports the idea that impaired mitochondrial function is a cause of the insulin insensitivity in different type of cells that arised as a result of an insufficient supply of energy or defects in the insulin signaling pathway. ROS are generally necessary for the proper functioning of the cell, but excessive ROS production can be harmful, which makes antioxidant defenses essential. Moreover, some substances with antioxidant properties, such as vitamin C or vitamin E, erradicate the oxidative stress associated with diabetes. The results of clinical trials employing anti-oxidative stress reagents in patients with diabetes are contradictory, which may be a result of inadequate study design or selected targets. This review considers the process of diabetes from a mitochondrial perspective, and describes the role of autophagy in the development of diabetes. Furthermore, we discuss the possible beneficial effects of selectively targeting antioxidants to mitochondria as a strategy for modulating mitochondrial function in diabetes. Keywords: Diabetes, mitochondria, oxidative stress, reactive oxygen species, insulin signaling pathway, vitamin C, vitamin E, autophagy, redox potential, transition metal ions
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