期刊
CURRENT PHARMACEUTICAL DESIGN
卷 20, 期 35, 页码 5653-5662出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1381612820666140306095717
关键词
Mitochondria; nitric oxide; carbon monoxide; H2S; HO-1; mitophagy
资金
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL108801] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI095424] Funding Source: NIH RePORTER
- Veterans Affairs [I01BX001926] Funding Source: NIH RePORTER
- NHLBI NIH HHS [P01 HL108801, P01-HL108801] Funding Source: Medline
- NIAID NIH HHS [R01 AI095424] Funding Source: Medline
- BLRD VA [I01 BX001926] Funding Source: Medline
The influence of mitochondrial dysfunction on pathological states involving inflammatory and/or oxidative stress in tissues that do not show frank cellular apoptosis or necrosis has been rather difficult to unravel, and the literature is replete with contradictory information. Although such discrepancies have many potential causes related to the type of injurious agent, the severity and duration of the injury, and the particular cells and tissues and the functions involved, it is the successful induction of cellular adaptive responses that ultimately governs the resolution of mitochondrial dysfunction and survival of the cell. Much recent attention has been devoted to unraveling the signaling pathways that activate mitochondrial biogenesis and other processes involved in mitochondrial quality control (QC) during inflammatory and oxidative stress with an eye towards the development of novel targets for therapeutic mitigation of the resultant tissue damage. This review provides a brief overview of this emerging field with an emphasis on the role of signaling through the endogenous gases (NO, CO and H2S) and a redox-based approach that brings transparency to key factors that contribute to the resolution of mitochondrial dysfunction and the maintenance of cell vitality. We make the case that targeted stimulation of mitochondrial biogenesis could be a potentially valuable approach for the development of new therapies for the treatment of diseases for which mitochondrial damage is a major consideration.
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