炎症
氧化应激
线粒体ROS
线粒体
生物
活性氧
免疫学
分区(防火)
细胞生物学
生物化学
酶
作者
Simone Patergnani,Esmaa Bouhamida,Sara Leo,Paolo Pinton,Alessandro Rimessi
出处
期刊:Biomedicines
[MDPI AG]
日期:2021-02-20
卷期号:9 (2): 216-216
被引量:65
标识
DOI:10.3390/biomedicines9020216
摘要
A decline in mitochondrial redox homeostasis has been associated with the development of a wide range of inflammatory-related diseases. Continue discoveries demonstrate that mitochondria are pivotal elements to trigger inflammation and stimulate innate immune signaling cascades to intensify the inflammatory response at front of different stimuli. Here, we review the evidence that an exacerbation in the levels of mitochondrial-derived reactive oxygen species (ROS) contribute to mito-inflammation, a new concept that identifies the compartmentalization of the inflammatory process, in which the mitochondrion acts as central regulator, checkpoint, and arbitrator. In particular, we discuss how ROS contribute to specific aspects of mito-inflammation in different inflammatory-related diseases, such as neurodegenerative disorders, cancer, pulmonary diseases, diabetes, and cardiovascular diseases. Taken together, these observations indicate that mitochondrial ROS influence and regulate a number of key aspects of mito-inflammation and that strategies directed to reduce or neutralize mitochondrial ROS levels might have broad beneficial effects on inflammatory-related diseases.
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