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Succinylation modification:a potential therapeutic target in stroke

Neural Regeneration Research 2024年第4期19卷 781-787页

作者： Jie Lian Wenwu Liu Qin Hu Xiaohua Zhang Department of Neurosurgery Ren Ji HospitalShanghai Jiao Tong University School of Medicine Department of Diving and Hyperbaric Medicine Naval Medical CenterNaval Medical University

Stroke is a leading cause of mortality and disability *** cell death triggered by the compromised supply of blood oxygen and glucose is one of the major pathophysiology of strokeinduced brain *** mitochondrial energy metabolism is observed minutes after stroke and is closely associated with the progression of ***,a new type of posttranslational modification,known as lysine succinylation,has been recognized to play a significant role in mitochondrial energy metabolism after ***,the role of succinylation modification in cell metabolism after stroke and its regulation are not well *** aimed to review the effects of succinylation on energy metabolism,reactive oxygen species generation,and neuroinflammation,as well as Sirtuin 5 mediated desuccinylation after *** also highlight the potential of targeting succinylation/desuccinylation as a promising strategy for the treatment of *** succinylation level is dynamically regulated by the nonenzymatic or enzymatic transfer of a succinyl group to a protein on lysine residues and the removal of succinyl catalyzed by *** evidence has suggested that succinylation can regulate the metabolic pathway through modulating the activity or stability of metabolic ***,especially Sirtuin 5,are characterized for their desuccinylation activity and have been recognized as a critical regulator of metabolism through desuccinylating numerous metabolic *** between succinylation and desuccinylation has been implicated in the pathophysiology of *** agents that enhance the activity of Sirtuin 5 have been employed to promote desuccinylation and improve mitochondrial metabolism,and neuroprotective effects of these agents have been observed in experimental stroke ***,their therapeutic efficacy in stroke patients should be validated.

关键词： mitochondria metabolism neuroprotection sirtuin 5 stroke succinylation modification

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mitochondrial dysfunction in type 2 diabetes:A neglected path to skeletal muscle atrophy

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World Journal of Orthopedics 2024年第2期15卷 101-104页

作者： Jian-Jun Wu Hui-Min Xian Da-Wei Yang Fan Yang Department of Cardiology The Second Affiliated Hospital of Harbin Medical UniversityHarbin 150001Heilongjiang ProvinceChina Department of Orthopedic Surgery The Fourth Affiliated Hospital of Harbin Medical UniversityHarbin 150001Heilongjiang ProvinceChina State Key Laboratory of Component-based Chinese Medicine Tianjin University of Traditional Chinese MedicineTianjin 30000China

Over the course of several decades,robust research has firmly established the significance of mitochondrial pathology as a central contributor to the onset of skeletal muscle atrophy in individuals with ***,the specific intricacies governing this process remain *** evidence highlights that individuals with diabetes regularly confront the severe consequences of skeletal muscle *** the sophisticated mechanisms at the core of this pathology requires a thorough and meticulous exploration into the nuanced factors intricately associated with mitochondrial dysfunction.

关键词： Mfn-2 Oxidative stress mitochondria metabolism Skeletal muscle atrophy Diabetes

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Oxidative stress and mitochondrial dysfunction of retinal ganglion cells injury exposures in long-term blue light

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International Journal of Ophthalmology(English edition) 2020年第12期13卷 1854-1863页

作者： Ke-Xin Guo Chen Huang Wei Wang Pei Zhang Ying Li Zi-Yuan Liu Min-Shu Wang Peking University Third Hospital Beijing 100191China Medical Research Center Peking University Third HospitalBeijing 100191China Department of Ophthalmology Peking University Third HospitalBeijing 100191China

AIM:To investigate the phototoxic effect of long-term excessive narrow-band blue light in staurosporine-induced differentiated retinal ganglion cells-5(SSRGC-5).METHODS:SSRGC-5 cells were divided into two groups,blue light group(BL group)and control *** viability was assessed by using CCK-8 *** profile analysis was performed by using Seahorse extracellular flux *** ultrastructure were studied via transmission electron microscope(TEM).mitochondria contents and oxidative stress was evaluated by flow *** blotting was performed to monitor the changes in mitogen-activated protein kinases(MAPK)pathway and PI3 K/AKT ***:Blue light caused morphological changes of SSRGC-5 *** cell viability was significantly decreased from 3 h in BL *** ROS and mitochondrial superoxide levels were increased following blue light *** profiling identified blue light induced SSRGC-5 cells to have severely compromised mitochondrial *** was accompanied by impaired mitochondrial ultrastructure and remodeling,increased expression of the mitochondrial related proteins,and increased glycolysis as ***,the results showed that blue light induced higher expression of p-p38,p38,p-JNK,p-ERK,p-cJun,c-Jun,and ***:These findings indicate that excessive narrow-band blue light induces oxidative stress and mitochondrial metabolic remodeling dysregulate in SSRGC-5 *** MAPK and AKT signaling pathways are involved in this process.

关键词： blue light retinal ganglion cell oxidative stress mitochondria metabolism mitochondria abnormalities mitogen-activated protein kinases AKT

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Effects of dichloroacetate on the activation of the mitochondrial pathway in C6 cells in vitro

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Journal of Chinese Pharmaceutical Sciences 2011年第5期20卷 460-465页

作者：赵欣王欣余克富段瑀李捷思赵炳祥张烜张强北京大学医学部药学院药剂学系北京100191 北京大学医学部天然药物及仿生药物国家重点实验室北京100191

mitochondria are increasingly recognized as important targets for tumor treatment because of their central roles in apoptotic pathways and cellular metabolism. Dichloroacetate （DCA）, a low molecular weight mitochondria-targeting agent, exhibits potential therapeutic effects for tumors. Based on the effects of DCA on tumor cellular metabolism, we carried out this study to investigate the anti-tumor activity of DCA in C6 glioma cells in vitro. The results showed that DCA was able to increase the activity of pyruvate dehydrogenase （PDH）, induce the production of reactive oxygen species （ROS） and reduce the mitochondrial membrane potential （MMP） in C6 ceils in vitro （P〈0.05 or 0.01）, indicating that the anti-tumor effects of DCA in C6 cells could be through the activation of the mitochondrial pathway. In conclusion, mitochondria could be a viable therapeutic target for the treatment of glioma.

关键词： mitochondria metabolism Dichloroacetate C6 glioma Pyruvate dehydrogenase Reactive oxygen species mitochondrial membrane potential

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