title: Reactive nitrogen species as therapeutic targets for autophagy: implication for ischemic stroke.
abstract: Roles of autophagy/mitophagy activation in ischemic stroke remain controversial. To elucidate potential reasons, we analyze the factors responsible for divergent results in literatures. Reactive nitrogen species (RNS) are important cytotoxic factors in ischemic stroke. Herein, we particularly discuss the roles played by RNS in autophagy/mitophagy and ischemic brain injury. Areas covered: Following factors should be considered in the studies on autophagy/mitophagy in ischemic stroke: (1) Protocols for administration of autophagy regulators including administration time points, routes and doses, etc.; (2) Specificity of autophagy regulators; (3) Animal models of cerebral ischemia with or without reperfusion. In the underlying mechanisms of autophagy/mitophagy, we particularly discuss the potential roles of RNS in mediating excessive autophagy/mitophagy during cerebral ischemia/reperfusion injury. Expert opinion: Emphasis should be given to the following aspects in future studies: (1) Targeting RNS and related cellular signaling pathways in the regulation of autophagy/mitophagy might be a promising strategy for developing novel drugs as well as combined therapy for thrombolytic treatment to reach better outcomes for ischemic stroke; (2) Developing circulating plasma biomarkers linking RNS-mediated autophagy/mitophagy to the magnitude of ischemic brain injury will benefit for stroke treatment. Subsequently, RNS could be dominant therapeutic targets to regulate autophagy/mitophagy for ischemic stroke.
authors.affiliation: a School of Chinese Medicine, LKS Faculty of Medicine , The University of Hong Kong , Hong Kong SAR , China.|b The University of Hong Kong-Shenzhen Institute of Research and Innovation (HKU-SIRI) , Shenzhen , China.
authors.forename: Jinghan
authors.initials: J
authors.lastname: Feng
authors.affiliation: a School of Chinese Medicine, LKS Faculty of Medicine , The University of Hong Kong , Hong Kong SAR , China.|b The University of Hong Kong-Shenzhen Institute of Research and Innovation (HKU-SIRI) , Shenzhen , China.
authors.forename: Xingmiao
authors.initials: X
authors.lastname: Chen
authors.affiliation: a School of Chinese Medicine, LKS Faculty of Medicine , The University of Hong Kong , Hong Kong SAR , China.|b The University of Hong Kong-Shenzhen Institute of Research and Innovation (HKU-SIRI) , Shenzhen , China.
authors.forename: Jiangang
authors.initials: J
authors.lastname: Shen
mesh_terms: D000818:Animals; D001343:Autophagy / Q000187:drug effects; D002545:Brain Ischemia / Q000188:drug therapy* / Q000503:physiopathology; D004195:Disease Models, Animal; D015195:Drug Design; D006801:Humans; D063306:Mitophagy / Q000187:drug effects; D058990:Molecular Targeted Therapy; D026361:Reactive Nitrogen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000188:drug therapy / Q000503:physiopathology; D020521:Stroke / Q000188:drug therapy* / Q000503:physiopathology; D015912:Thrombolytic Therapy / Q000379:methods
chemical_list: D026361:Reactive Nitrogen Species
keywords: Autophagy; ischemic stroke; mitochondria; mitophagy; programmed cell death; reactive nitrogen species