Role of SIRT1-Mediated Reactive Oxygen Species and Neuroinflammation in Stroke
1Beijing Friendship Hospital, Beijing, China
2Johns Hopkins University, Baltimore, USA
3Jinling Hospital Medical School of Nanjing University, Nanjing, China
4Nanjing Drum Tower Hospital, Nanjing, China
Role of SIRT1-Mediated Reactive Oxygen Species and Neuroinflammation in Stroke
Description
A stroke is a fatal cerebral vascular disease with high morbidity and mortality rate in most countries. With the occurrence of hemorrhage and ischemia, reactive oxygen species (ROS) overproduction and neuroinflammation have been implicated in the subsequent brain injury. ROS can elicit a plethora of detrimental effects on cellular functions by causing damages to proteins, lipids, and nucleic acids. In addition, ROS overproduction is closely associated with neuroinflammation and each of them promotes and amplifies the other one. Therefore, there is a pressing need to find new therapeutic targets for stroke.
SIRT1, a member of the sirtuin family, plays a prominent role in regulating various biological functions, such as immune response, apoptosis, oxidative stress, and aging. The function of SIRT1 is increasingly recognized as especially important in the pathogenesis of neurological diseases. At the cellular level, SIRT1 is known as a nuclear protein, which is predominantly expressed in neurons. Upon activation, SIRT1 can modulate a variety of signaling pathways to affect oxidative stress and inflammation, including nuclear factor-erythroid 2-related factor 2, nod-like receptor pyrin domain-containing 3 inflammasome, forkhead transcription factors of the O class, and NADPH oxidases. Targeting the SIRT1 to reduce ROS and neuroinflammation might represent an emerging therapeutic target for stroke. However, the current therapeutics studies always ignore the crosstalk between ROS and neuroinflammation mediated by SIRT1.
The aim of this Special Issue is to collate original research and review articles about the SIRT1-mediated mechanisms, signaling pathways, and corresponding therapeutics in oxidative stress and neuroinflammation after stroke.
Potential topics include but are not limited to the following:
- Novel underlying mechanisms of SIRT1 in the pathophysiological processes of stroke
- The interplay between ROS and neuroinflammation
- Effect of compounds and natural drugs on SIRT1 signaling related to oxidative stress and neuroinflammation
- New therapeutic strategies targeting oxidative stress and neuroinflammation for the treatment of stroke
- Translational research for the treatment of strokes related to SIRT1 signaling