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mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage

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Neural Regeneration Research 2024年第4期19卷 825-832页

作者： Jiatong Zhang Qi Zhu Jie Wang Zheng Peng Zong Zhuang Chunhua Hang Wei Li Department of Neurosurgery Nanjing Drum Tower HospitalAffiliated Hospital of Medical SchoolNanjing University Department of Neurosurgery Nanjing Drum Tower HospitalClinical College of Nanjing Medical University

The dramatic increase in intracranial pressure after subarachnoid hemorrhage leads to a decrease in cerebral perfusion pressure and a reduction in cerebral blood *** are directly affected by direct factors such as ischemia,hypoxia,excitotoxicity,and toxicity of free hemoglobin and its degradation products,which trigger mitochondrial *** mitochondria release large amounts of reactive oxygen species,inflammatory mediators,and apoptotic proteins that activate apoptotic pathways,further damaging *** response to this array of damage,cells have adopted multiple mitochondrial quality control mechanisms through evolution,including mitochondrial protein quality control,mitochondrial dynamics,mitophagy,mitochondrial biogenesis,and intercellular mitochondrial transfer,to maintain mitochondrial homeostasis under pathological *** interventions targeting mitochondrial quality control mechanisms have emerged as promising therapeutic strategies for subarachnoid *** review provides an overview of recent research advances in mitochondrial pathophysiological processes after subarachnoid hemorrhage,particularly mitochondrial quality control *** also presents potential therapeutic strategies to target mitochondrial quality control in subarachnoid hemorrhage.

关键词： mitochondrial biogenesis mitochondrial dynamics mitochondrial dysfunction mitochondrial fission and fusion mitochondrial quality control mitophagy subarachnoid hemorrhage

mitochondrial dysfunction in glaucomatous degeneration

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International Journal of Ophthalmology(English edition) 2023年第5期16卷 811-823页

作者： Zi-Qiao Zhang Zhi Xie Sen-Yuan Chen Xu Zhang Affiliated Eye Hospital of Nanchang University Nanchang University School of Ophthalmology&OptometryJiangxi Provincial Key Laboratory for OphthalmologyJiangxi Research Institute of Ophthalmology&Visual ScienceNanchang 330006Jiangxi ProvinceChina Queen Mary School Nanchang UniversityNanchang 330006Jiangxi ProvinceChina

Glaucoma is a kind of optic neuropathy mainly manifested in the permanent death of retinal ganglion cells(RGCs),atrophy of the optic nerve,and loss of visual *** main risk factors for glaucoma consist of the pathological elevation of intraocular pressure(IOP)and *** the mechanism of glaucoma remains an open question,a theory related to mitochondrial dysfunction has been emerging in the last *** oxygen species(ROS)from the mitochondrial respiratory chain are abnormally produced as a result of mitochondrial *** stress takes place when the cellular antioxidant system fails to remove excessive ROS ***,more and more studies show that there are other common features of mitochondrial dysfunction in glaucoma,including damage of mitochondrial DNA(mt DNA),defective mitochondrial quality control,ATP reduction,and other cellular changes,which are worth summarizing and further *** purpose of this review is to explore mitochondrial dysfunction in the mechanism of glaucomatous optic *** on the mechanism,the existing therapeutic options are summarized,including medications,gene therapy,and red-light therapy,which are promising to provide feasible neuroprotective ideas for the treatment of glaucoma.

关键词： glaucoma mitochondrial dysfunction oxidative stress mitochondrial dynamics mitophagy neuroprotection

Nicotine-induced transcriptional changes and mitochondrial dysfunction in the ventral tegmental area revealed by single-nucleus transcriptomics

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Journal of Genetics and Genomics 2024年第11期51卷 1237-1251页

作者： Lei Fan Boxin Liu Ru Yao Xia Gao Hongjuan Wang Sanjie Jiang Xiaomin Zheng Huan Chen Hongwei Hou Yong Liu Qingyuan Hu Anhui Institute of Optics and Fine Mechanics Hefei Institutes of Physical ScienceChinese Academy of SciencesHefeiAnhui 230000China University of Science and Technology of China HefeiAnhui 230000China Beijing Life Science Academy Beijing 100000China Key Laboratory of Tobacco Biological Effects and Biosynthesis Bejing 100000China China National Tobacco Quality Supervision&Test Center ZhengzhouHenan 450000China Key Laboratory of Tobacco Biological Effects ZhengzhouHenan 450000China BGI Genomics BGI-ShenzhenGuangdong 518018China

Nicotine is widely recognized as the primary contributor to tobacco *** studies have indicated that molecular and behavioral responses to nicotine are primarily mediated by ventral tegmental area(VTA)neurons,and accumulating evidence suggests that glia play prominent roles in nicotine ***,VTA neurons and glia have yet to be characterized at the transcriptional level during the progression of nicotine ***,a male mouse model of nicotine self-administration is established and the timing of three critical phases(pre-addiction,addicting,and post-addiction phase)is ***-nucleus RNA sequencing in the VTA at each phase is performed to comprehensively classify specific cell *** changes occurred during the addicting and post-addiction phases,with the addicting phase displaying highly dynamic neuroplasticity that profoundly impacts the transcription in each cell ***,significant transcriptional changes in energy metabolism-related genes are observed,accompanied by notable structural alterations in neuronal mitochondria during the progression of nicotine *** results provide insights into mechanisms underlying the progression of nicotine addiction,serving as an important resource for identifying potential molecular targets for nicotine cessation.

关键词： Single-nucleus transcriptomics Ventral tegmental area Nicotine addiction Cell-type-specific alteration mitochondrial dysfunction

SARM1 participates in axonal degeneration and mitochondrial dysfunction in prion disease

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Neural Regeneration Research 2022年第10期17卷 2293-2299页

作者： Meng-Yu Lai Jie Li Xi-Xi Zhang Wei Wu Zhi-Ping Li Zhi-Xin Sun Meng-Yang Zhao Dong-Ming Yang Dong-Dong Wang Wen Li De-Ming Zhao Xiang-Mei Zhou Li-Feng Yang National Animal Transmissible Spongiform Encephalopathy Laboratory College of Veterinary MedicineChina Agricultural UniversityBeijingChina

Prion disease represents a group of fatal neurogenerative diseases in humans and animals that are associated with energy loss,axonal degeneration,and mitochondrial *** degeneration is an early hallmark of neurodegeneration and is triggered by *** found that depletion or dysfunctional mutation of SARM1 protected against NAD+loss,axonal degeneration,and mitochondrial functional disorder induced by the neurotoxic peptide ***+supplementation rescued prion-triggered axonal degeneration and mitochondrial dysfunction and SARM1 overexpression suppressed this protective ***+supplementation in PrP106-126-incubated N2a cells,SARM1 depletion,and SARM1 dysfunctional mutation each blocked neuronal apoptosis and increased cell *** results indicate that the axonal degeneration and mitochondrial dysfunction triggered by PrP^(106-126) are partially dependent on SARM1 NADase *** pathway has potential as a therapeutic target in the early stages of prion disease.

关键词： axonal degeneration mitochondrial dysfunction NAD+metabolism NADase neurodegenerative disease prion disease SARM1 sterile alpha and TIR motif-containing 1

Selenoproteins synergistically protect porcine skeletal muscle from oxidative damage via relieving mitochondrial dysfunction and endoplasmic reticulum stress

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Journal of Animal Science and Biotechnology 2023年第5期14卷 2180-2196页

作者： Jinzhong Jing Ying He Yan Liu Jiayong Tang Longqiong Wang Gang Jia Guangmang Liu Xiaoling Chen Gang Tian Jingyi Cai Lianqiang Che Bo Kang Hua Zhao Key Laboratory for Animal Disease‑Resistance Nutrition of Ministry of Education of China Ministry of Agriculture and Rural Affairsof Sichuan ProvinceAnimal Nutrition InstituteSichuan Agricultural UniversityChengdu 611130SichuanChina College of Animal Science and Technology Sichuan Agricultural UniversityChengdu 611130SichuanChina

Background The skeletal muscle of pigs is vulnerable to oxidative damage,resulting in growth *** are important components of antioxidant systems for animals,which are generally regulated by dietary selenium(Se)***,we developed the dietary oxidative stress(DOS)-inducing pig model to investigate the protective effects of selenoproteins on DOS-induced skeletal muscle growth *** Dietary oxidative stress caused porcine skeletal muscle oxidative damage and growth retardation,which is accompanied by mitochondrial dysfunction,endoplasmic reticulum(ER)stress,and protein and lipid metabolism *** with Se(0.3,0.6 or 0.9 mg Se/kg)in form of hydroxy selenomethionine(OH-SeMet)linearly increased muscular Se deposition and exhibited protective effects via regulating the expression of selenotranscriptome and key selenoproteins,which was mainly reflected in lower ROS levels and higher antioxidant capacity in skeletal muscle,and the mitigation of mitochondrial dysfunction and ER ***’s more,selenoproteins inhibited DOS induced protein and lipid degradation and improved protein and lipid biosynthesis via regulating AKT/mTOR/S6K1 and AMPK/SREBP-1 signalling pathways in skeletal ***,several parameters such as the activity of GSH-Px and T-SOD,the protein abundance of JNK2,CLPP,SELENOS and SELENOF did not show dose-dependent ***,several key selenoproteins such as MSRB1,SELENOW,SELENOM,SELENON and SELENOS play the unique roles during this *** Increased expression of selenoproteins by dietary OH-SeMet could synergistically alleviate mitochondrial dysfunction and ER stress,recover protein and lipid biosynthesis,thus alleviate skeletal muscle growth *** study provides preventive measure for OS-dependent skeletal muscle retardation in livestock husbandry.

关键词： Dietary oxidative stress Endoplasmic reticulum stress Growth retardation mitochondrial dysfunction Selenoproteins Skeletal muscle

Protein profiling identified mitochondrial dysfunction and synaptic abnormalities after dexamethasone intervention in rats with traumatic brain injury

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Neural Regeneration Research 2021年第12期16卷 2438-2445页

作者： Fei Niu Bin Zhang Jie Feng Xiang Mao Xiao-Jian Xu Jin-Qian Dong Bai-Yun Liu Department of Neurotrauma Beijing Key Laboratory of Central Nervous System InjuryBeijing Neurosurgical InstituteCapital Medical UniversityBeijingChina Department of Neurosurgery Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Key Laboratory of Central Nervous System Injury Research Center for Brain TumorBeijing Institute of Brain DisordersBeijing Neurosurgical InstituteCapital Medical UniversityBeijingChina Department of Neurosurgery the First Affiliated Hospital of Anhui Medical UniversityHefeiAnhui ProvinceChina Center for Nerve Injury and Repair Beijing Institute of Brain DisordersBeijingChina China National Clinical Research Center for Neurological Diseases BeijingChina

Dexamethasone has been widely used after various neurosurgical procedures due to its anti-inflammatory property and the abilities to restore vascular permeability,inhibit free radicals,and reduce cerebrospinal fluid *** to the latest guidelines for the treatment of traumatic brain injury in the United States,high-dose glucocorticoids cause neurological *** investigate the reason why high-dose glucocorticoids after traumatic brain injury exhibit harmful effect,rat controlled cortical impact models of traumatic brain injury were *** 1 hour and 2 days after surgery,rat models were intraperitoneally administered dexamethasone 10 mg/*** results revealed that 31 proteins were significantly upregulated and 12 proteins were significantly downregulated in rat models of traumatic brain injury after dexamethasone *** Ingenuity Pathway Analysis results showed that differentially expressed proteins were enriched in the mitochondrial dysfunction pathway and synaptogenesis signaling *** blot analysis and immunohistochemistry results showed that Ndufv2,Maob and Gria3 expression and positive cell count in the dexamethasone-treated group were significantly greater than those in the model *** findings suggest that dexamethasone may promote a compensatory increase in complex I subunits(Ndufs2 and Ndufv2),increase the expression of mitochondrial enzyme Maob,and upregulate synaptic-transmission-related protein *** changes may be caused by nerve injury after traumatic brain injury treatment by *** study was approved by Institutional Ethics Committee of Beijing Neurosurgical Institute(approval No.201802001)on June 6,2018.

关键词： dexamethasone Gria3 Maob mass spectrometry mitochondrial dysfunction Ndufs2 Ndufv2 proteomics synaptic abnormalities traumatic brain injury

mitochondrial dysfunction and cellularmetabolic deficiency in Alzheimer's disease

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Neuroscience Bulletin 2012年第5期28卷 631-640页

作者： Xue-Mei Gu Han-Chang Huang Zhao-Feng Jiang Beijing Military General Hospital Beijing 100700 China Beijing Key Laboratory of Bioactive Substances and Functional Foods Beijing Union University Beijing 100191 China College of Life Science and Technology Beijing University of Chemical Technology Beijing 100029 China

Alzheimer＇s disease （AD） is an age-related neurodegenerative disorder. The pathology of AD includes amyloid-β （Aβ） deposits in neuritic plaques and neurofibrillary tangles composed of hyperphosphorylated tau, as well as neuronal loss in specific brain regions. Increasing epidemiological and functional neuroimaging evidence indicates that global and regional disruptions in brain metabolism are involved in the pathogenesis of this disease. Aβ precursor protein is cleaved to produce both extracellular and intracellular Aβ, accumulation of which might interfere with the homeostasis of cellular metabolism. Mitochondria are highly dynamic organelles that not only supply the main energy to the cell but also regulate apoptosis. mitochondrial dysfunction might contribute to Aβ neurotoxicity. In this review, we summarize the pathways ofAβ generation and its potential neurotoxic effects on cellular metabolism and mitochondrial dysfunction.

关键词： Alzheimer’s disease amyloid-β metabolic deficiency mitochondrial dysfunction

Selenomethionine alleviates chronic heat stress-induced breast muscle injury and poor meat quality in broilers via relieving mitochondrial dysfunction and endoplasmic reticulum stress

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Animal Nutrition 2024年第1期16卷 363-375页

作者： Jinzhong Jing Jiayi Wang Xiaoyu Xiang Shenggang Yin Jiayong Tang Longqiong Wang Gang Jia Guangmang Liu Xiaoling Chen Gang Tian Jingyi Cai Bo Kang Lianqiang Che Hua Zhao Key Laboratory for Animal Disease-Resistance Nutrition of Ministry of Education of China Ministry of Agriculture and Rural Affairsof Sichuan ProvinceAnimal Nutrition InstituteSichuan Agricultural UniversityChengdu 611130SichuanChina College of Animal Science and Technology Sichuan Agricultural UniversityChengdu 611130SichuanChina

In the present study,the chronic heat stress(CHS)broiler model was developed to investigate the potential protection mechanism of organic selenium(selenomethionine,SeMet)on CHS-induced skeletal muscle growth retardation and poor meat *** hundred Arbor Acres male broilers(680±70 g,21 d old)were grouped into 5 treatments with 8 replicates of 10 broilers per *** in the control group were raised in a thermoneutral environment(22±2°C)and fed with a basal *** other four treatments were exposed to hyperthermic conditions(33±2°C,24 h in each day)and fed on the basal diet supplied with SeMet at 0.0,0.2,0.4,and 0.6 mg Se/kg,respectively,for 21 *** showed that CHS reduced(Pmitochondrial stress and endoplasmic reticulum(ER)stress in breast muscle,which increased(Pmitochondrial stress and ER ***'s more,SeMet suppressed protein degradation and improved protein biosynthesis though inhibiting the caspase and ubiquitin proteasome system and promoting the mTOR-4EBP1 *** conclusion,dietary SeMet supplementation increases the expression of several key selenoproteins

关键词： Broiler Chronic heat stress Skeletal muscle Meat quality mitochondrial dysfunction Endoplasmic reticulum stress

Neuroprotective effects of curculigoside against Alzheimer’s disease via regulation oxidative stress mediated mitochondrial dysfunction in L-Glu-exposed HT22 cells and APP/PS1 mice

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Food Science and Human Wellness 2023年第4期12卷 1265-1278页

作者： Wenqi Wang Yidi Qu Siyu Li Jinyu Chu Hongxin Yang Lirong Teng Di Wang School of Life Sciences Jilin UniversityChangchun 130012China

Curculigoside(CCG)is a phenolic glycoside compound extracted from the root of a natural plant called Curculigo orchioides *** this study,the neuroprotective effect of CCG through oxidative stress mediated mitochondrial dysfunction on L-glutamate(L-Glu)-damaged hippocampal neuron cell line(HT22)and APPswe/PSEN1dE9 transgenic(APP/PS1)mice were ***,CCG in L-Glu-damaged HT22 cells suppressed apoptosis,reduced the accumulation of reactive oxygen species,balanced the mitochondrial membrane potential and prevented the over-influx of *** APP/PS1 mice,4-week CCG administration significantly improved their memory and behavioral impairments,enhanced the function of cholinergic system,reduced the deposition of Aβand neurofibrillary fiber tangles caused by tau phosphorylation,and suppressed the development and progression of oxidative stress in brains of APP/PS1 *** on the screening of proteomic analysis on hippocampus,CCG were confirmed that it could regulate the expression levels of proteins related to mitochondrial dysfunction,mainly through activating on AMPK/Nrf2 signaling,in APP/PS1 mice and L-Glu-exposed HT22 *** has a prominent neuroprotective effect on regulate the AMPK/Nrf2-mediated mitochondrial dysfunction in cells APP/PS1 mice support CCG is a potentially potent drug for AD treatment and merits further investigation.

关键词： Alzheimer’s disease Curculigoside Apoptosis Oxidative stress mitochondrial dysfunction AMPK/Nrf2 signaling