期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 171, 期 -, 页码 345-364出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2021.05.013
关键词
Mitochondria; Reactive oxygen species; NADPH oxidases; Heart failure; Redox signaling
资金
- Deutsche Forschungsgemeinschaft (DFG) [Ma 2528/7-1, SFB 894, TRR-219]
- Federal Ministry of Education and Research (BMBF) [01EO1504]
- Barth Syndrome Foundation
Heart failure is a growing health burden globally, characterized by alterations in excitation-contraction coupling, cardiac energy deficit, and oxidative stress. While targeting metabolism may provide prognostic benefits, treatments specifically targeting reactive oxygen species (ROS) are still in preclinical stages. More research is needed in this area to develop effective therapies for heart failure.
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据