活性氧
氧化应激
心力衰竭
线粒体ROS
线粒体
黄嘌呤氧化酶
细胞生物学
NADPH氧化酶
活性氮物种
生物
医学
化学
生物信息学
内科学
生物化学
酶
作者
David E. Weissman,Christoph Maack
标识
DOI:10.1016/j.freeradbiomed.2021.05.013
摘要
Heart failure is a growing health burden worldwide characterized by alterations in excitation-contraction coupling, cardiac energetic deficit and oxidative stress. While current treatments are mostly limited to antagonization of neuroendocrine activation, more recent data suggest that also targeting metabolism may provide substantial prognostic benefit. However, although in a broad spectrum of preclinical models, oxidative stress plays a causal role for the development and progression of heart failure, no treatment that targets reactive oxygen species (ROS) directly has entered the clinical arena yet. In the heart, ROS derive from various sources, such as NADPH oxidases, xanthine oxidase, uncoupled nitric oxide synthase and mitochondria. While mitochondria are the primary source of ROS in the heart, communication between different ROS sources may be relevant for physiological signalling events as well as pathologically elevated ROS that deteriorate excitation-contraction coupling, induce hypertrophy and/or trigger cell death. Here, we review the sources of ROS in the heart, the modes of pathological activation of ROS formation as well as therapeutic approaches that may target ROS specifically in mitochondria.
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