检索结果-南通市图书馆

mitophagy links oxidative stress conditions and neurodegenerative diseases

Neural Regeneration Research 2019年第5期14卷 749-756页

作者： Ulfuara Shefa Na Young Jeong In Ok Song Hyung-Joo Chung Dokyoung Kim Junyang Jung Youngbuhm Huh Department of Biomedical Science Graduate School Kyung Hee University Department of Anatomy and Cell Biology College of Medicine Dong-A University Department of Reproductive Endocrinology and Infertility Department of Obstetrics and Gynecology Cheil General Hospital Dankook University College of Medicine Department of Anesthesiology and Pain Medicine College of Medicine Kosin University Department of Anatomy and Neurobiology College of Medicine Kyung Hee University

mitophagy is activated by a number of stimuli, including hypoxia, energy stress, and increased oxidative phosphorylation activity. mitophagy is associated with oxidative stress conditions and central neurodegenerative diseases. Proper regulation of mitophagy is crucial for maintaining homeostasis; conversely, inadequate removal of mitochondria through mitophagy leads to the generation of oxidative species, including reactive oxygen species and reactive nitrogen species, resulting in various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. These diseases are most prevalent in older adults whose bodies fail to maintain proper mitophagic functions to combat oxidative species. As mitophagy is essential for normal body function, by targeting mitophagic pathways we can improve these disease conditions. The search for effective remedies to treat these disease conditions is an ongoing process, which is why more studies are needed. Additionally, more relevant studies could help establish therapeutic conditions, which are currently in high demand. In this review, we discuss how mitophagy plays a significant role in homeostasis and how its dysregulation causes neurodegeneration. We also discuss how combating oxidative species and targeting mitophagy can help treat these neurodegenerative diseases.

关键词： nerve regeneration mitophagy central nervous system Alzheimer’s disease Parkinson’s disease Huntington’s disease amyotrophic lateral sclerosis oxidative species reactive oxygen species reactive nitrogen species

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

ROS-mediated BNIP3-dependent mitophagy promotes coelomocyte survival in Apostichopus japonicus in response to Vibrio splendidus infection

引用

Zoological Research 2022年第2期43卷 285-300页

作者： Lian-Lian Sun Yi-Na Shao Mei-Xiang You Cheng-Hua Li State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products Ningbo UniversityNingboZhejiang 315211China Laboratory for Marine Fisheries Science and Food Production Processes Qingdao National Laboratory for Marine Science and TechnologyQingdaoShandong 266071China State-Province Joint Laboratory of Marine Biotechnology and Engineering Ningbo UniversityNingboZhejiang 315211China

Organisms produce high levels of reactive oxygen species(ROS)to kill pathogens or act as signaling molecules to induce immune responses;however,excessive ROS can result in cell death.To maintain ROS balance and cell survival,mitophagy selectively eliminates damaged mitochondria via mitophagy receptors in vertebrates.In marine invertebrates,however,mitophagy and its functions remain largely unknown.In the current study,Vibrio splendidus infection damaged mitochondrial morphology in coelomocytes and reduced mitochondrial membrane potential(ΔΨm)and mitophagosome formation.The colocalization of mitochondria and lysosomes further confirmed that lipopolysaccharide(LPS)treatment increased mitophagy flux.To explore the regulatory mechanism of mitophagy,we cloned Bcl2/adenovirus E1 B 19 kDa protein-interacting protein 3(BNIP3),a common mitophagy receptor,from sea cucumber Apostichopus japonicus(Aj BNIP3)and confirmed that Aj BNIP3 was significantly induced and accumulated in mitochondria after V.splendidus infection and LPS exposure.At the mitochondrial membrane,Aj BNIP3 interacts with microtubule-associated protein 1 light chain 3(LC3)on phagophore membranes to mediate mitophagy.After Aj BNIP3 interference,mitophagy flux decreased significantly.Furthermore,Aj BNIP3-mediated mitophagy was activated by ROS following the addition of exogenous hydrogen peroxide(H2 O2),ROS scavengers,and ROS inhibitors.Finally,inhibition of BNIP3-mediated mitophagy by Aj BNIP3 small interfering RNA(si RNA)or high concentrations of lactate increased apoptosis and decreased coelomocyte survival.These findings highlight the essential role of Aj BNIP3 in damaged mitochondrial degradation during mitophagy.This mitophagy activity is required for coelomocyte survival in A.japonicus against V.splendidus infection.

关键词： Apostichopus japonicus mitophagy Bcl2/adenovirus E1B 19 kDa protein-interacting protein 3 Reactive oxygen species Microtubule-associated protein 1 light chain 3

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Role of mitophagy in Myocardial Ischemia/Reperfusion Injury and Chinese Medicine Treatment

引用

Chinese Journal of Integrative Medicine 2023年第1期29卷 81-88页

作者： XIA Jun-yan CHEN Cong LIN Qian CUI Jie WAN Jie LI Yan LI Dong Department of Cardiology Dongfang Hospitalthe Second Affiliated Hospital of Beijing University of Chinese MedicineBeijing100078China Department of Cardiology Dongzhimen Hospitalthe First Affiliated Hospital of Beijing University of Chinese MedicineBeijing100007China

mitophagy is one of the important targets for the prevention and treatment of myocardial ischemia/reperfusion injury(MIRI).Moderate mitophagy can remove damaged mitochondria,inhibit excessive reactive oxygen species accumulation,and protect mitochondria from damage.However,excessive enhancement of mitophagy greatly reduces adenosine triphosphate production and energy supply for cell survival,and aggravates cell death.How dysfunctional mitochondria are selectively recognized and engulfed is related to the interaction of adaptors on the mitochondrial membrane,which mainly include phosphatase and tensin homolog deleted on chromosome ten(PTEN)-induced kinase 1/Parkin,hypoxia-inducible factor-1α/Bcl-2 and adenovirus e1b19k Da interacting protein 3,FUN-14 domain containing protein 1 receptor-mediated mitophagy pathway and so on.In this review,the authors briefly summarize the main pathways currently studied on mitophagy and the relationship between mitophagy and MIRI,and incorporate and analyze research data on prevention and treatment of MIRI with Chinese medicine,thereby provide relevant theoretical basis and treatment ideas for clinical prevention of MIRI.

关键词： mitophagy myocardial ischemia/reperfusion injury PTEN-induced kinase 1/Parkin hypoxia-inducible factor-1α/Bcl-2 and adenovirus e1b19k Da interacting protein 3 FUN-14 domain containing protein 1 Chinese medicine

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Histone deacetylase inhibitors inhibit cervical cancer growth through Parkin acetylationmediated mitophagy

引用

Acta Pharmaceutica Sinica B 2022年第2期12卷 838-852页

作者： Xin Sun Yuhan Shu Guiqin Ye Caixia Wu Mengting Xu Ruilan Gao Dongsheng Huang Jianbin Zhang Department of Oncology Cancer Center of Zhejiang Provincial People’s HospitalAffiliated People’s HospitalHangzhou Medical CollegeHangzhou 310014China Clinical Research Institute Zhejiang Provincial People’s HospitalAffiliated People’s HospitalHangzhou Medical CollegeHangzhou 310014China Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province Hangzhou Medical CollegeHangzhou 310014China College of Biomedical Engineering&Instrument Science Zhejiang UniversityHangzhou 310028China Department of Hematology the First Affiliated Hospital of Zhejiang Chinese Medical UniversityHangzhou 310006China

Parkin,an E3 ubiquitin ligase,plays a role in maintaining mitochondrial homeostasis through targeting damaged mitochondria for mitophagy.Accumulating evidence suggests that the acetylation modification of the key mitophagy machinery influences mitophagy level,but the underlying mechanism is poorly understood.Here,our study demonstrated that inhibition of histone deacetylase(HDAC)by treatment of HDACis activates mitophagy through mediating Parkin acetylation,leading to inhibition of cervical cancer cell proliferation.Bioinformatics analysis shows that Parkin expression is inversely correlated with HDAC2 expression in human cervical cancer,indicating the low acetylation level of Parkin.Using mass spectrometry,Parkin is identified to interact with two upstream molecules,acetylase acetyl-Co A acetyltransferase 1(ACAT1)and deacetylase HDAC2.Under treatment of suberoylanilide hydroxamic acid(SAHA),Parkin is acetylated at lysine residues 129,220 and 349,located in different domains of Parkin protein.In in vitro experiments,combined mutation of Parkin largely attenuate the interaction of Parkin with PTEN induced putative kinase 1(PINK1)and the function of Parkin in mitophagy induction and tumor suppression.In tumor xenografts,the expression of mutant Parkin impairs the tumor suppressive effect of Parkin and decreases the anticancer activity of SAHA.Our results reveal an acetylation-dependent regulatory mechanism governing Parkin in mitophagy and cervical carcinogenesis,which offers a new mitophagy modulation strategy for cancer therapy.

关键词： Parkin mitophagy ACAT1 HDAC2 Acetylation Ubiquitination Tumor suppression Cervical cancer

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Role of mitophagy in the hallmarks of aging

引用

The Journal of Biomedical Research 2023年第1期37卷 1-14页

作者： Jie Wen Tingyu Pan Hongyan Li Haixia Fan Jinhua Liu Zhiyou Cai Bin Zhao Department and Institute of Neurology Guangdong Medical UniversityZhanjiangGuangdong 524001China Guangdong Key Laboratory of Aging-related Cardiac and Cerebral Diseases ZhanjiangGuangdong 524001China Chongqing Key Laboratory of Neurodegenerative Diseases Chongqing 400013China Department of Neurology Chongqing General HospitalChongqing 400013China Department of Neurology the Affiliated Hospital of Southwest Medical UniversityLuzhouSichuan 646000China Chongqing Medical University Chongqing 400042China

Aging, subjected to scientific scrutiny, is extensively defined as a time-dependent decline in functions that involves the majority of organisms. The time-dependent accretion of cellular lesions is generally a universal trigger of aging, while mitochondrial dysfunction is a sign of aging. Dysfunctional mitochondria are identified and removed by mitophagy, a selective form of macroautophagy. Increased mitochondrial damage resulting from reduced biogenesis and clearance may promote the aging process. The primary purpose of this paper is to illustrate in detail the effects of mitophagy on aging and emphasize the associations between mitophagy and other signs of aging, including dietary restriction, telomere shortening, epigenetic alterations, and protein imbalance.The evidence regarding the effects of these elements on aging is still limited. And although the understanding of relationship between mitophagy and aging has been long-awaited, to analyze details of such a relationship remains the main challenge in aging studies.

关键词： mitophagy aging dietary restriction telomere shortening epigenetic alterations protein imbalance

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Insight into Crosstalk Between mitophagy and Apoptosis/Necroptosis:Mechanisms and Clinical Applications in Ischemic Stroke

引用

Current Medical Science 2022年第2期42卷 237-248页

作者： Yan-di YANG Zi-xin LI Xi-min HU Hao WAN Qi ZHANG Rui XIAO Kun XIONG Department of Anatomy and Neurobiology School of Basic Medical ScienceCentral South UniversityChangsha 410013China Clinical Medicine Eight-year Program 03 Class18 GradeXiangya School of MedicineCentral South UniversityChangsha 410013China Clinical Medicine Eight-Year Program 02 Class17 GradeXiangya School of MedicineCentral South UniversityChangsha 410013China Administrative Office the Third Xiangya HospitalCentral South UniversityChangsha 410013China Hunan Key Laboratory of Ophthalmology Changsha 410008China Key Laboratory of Emergency and Trauma Ministry of EducationCollege of Emergency and TraumaHainan Medical UniversityHaikou 571199China

Ischemic stroke is a serious cerebrovascular disease with high morbidity and mortality.As a result of ischemia-reperfusion,a cascade of pathophysiological responses is triggered by the imbalance in metabolic supply and demand,resulting in cell loss.These cellular injuries follow various molecular mechanisms solely or in combination with this disorder.Mitochondria play a driving role in the pathophysiological processes of ischemic stroke.Once ischemic stroke occurs,damaged cells would respond to such stress through mitophagy.mitophagy is known as a conservatively selective autophagy,contributing to the removal of excessive protein aggregates and damaged intracellular components,as well as aging mitochondria.Moderate mitophagy may exert neuroprotection against stroke.Several pathways associated with the mitochondrial network collectively contribute to recovering the homeostasis of the neurovascular unit.However,excessive mitophagy would also promote ischemia-reperfusion injury.Therefore,mitophagy is a double-edged sword,which suggests that maximizing the benefits of mitophagy is one of the direction of future efforts.This review emphasized the role of mitophagy in ischemic stroke,and highlighted the crosstalk between mitophagy and apoptosis/necroptosis.

关键词： mitophagy ischemic stroke apoptosis necroptosis clinical application crosstalk

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Defective mitophagy and the etiopathogenesis of Alzheimer’s disease

引用

Translational Neurodegeneration 2022年第1期11卷 461-473页

作者： Kuan Zeng Xuan Yu Yacoubou Abdoul Razak Mahaman Jian-Zhi Wang Rong Liu Yi Li Xiaochuan Wang Department of Psychiatry Wuhan Mental Health CenterWuhan 430012China Co-Innovation Center of Neurodegeneration Nantong UniversityNantong 226001China Department of Pathophysiology School of Basic MedicineKey Laboratory of Education Ministry/Hubei Province of China for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Wuhan Hospital for Psychotherapy Wuhan 430012China Shenzhen Huazhong University of Science and Technology Research Institute Shenzhen 518000China.

Accumulation of impaired mitochondria and energy metabolism disorders are non-negligible features of both aging and age-related neurodegeneration,including Alzheimer’s disease(AD).A growing number of studies suggest that mitophagy disorders play an important role in AD occurrence and development.The interaction between mitophagy deficits and Aβor Tau pathology may form a vicious cycle and cause neuronal damage and death.Elucidating the molecular mechanism of mitophagy and its role in AD may provide insights into the etiology and mechanisms of AD.Defective mitophagy is a potential target for AD prevention and treatment.

关键词： mitophagy Alzheimer’s disease PINK1 Tau Aβ

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

mitophagy in intracerebral hemorrhage:a new target for therapeutic intervention

引用

Neural Regeneration Research 2024年第2期19卷 316-323页

作者： Yiyang Chen Wenxuan Tang Xinqi Huang Yumei An Jiawen Li Shengye Yuan Haiyan Shan Mingyang Zhang Institute of Forensic Sciences Suzhou Medical CollegeSoochow UniversitySuzhouJiangsu ProvinceChina Shanghai Key Lab of Forensic Medicine Key Lab of Forensic ScienceMinistry of Justice(Academy of Forensic Science)ShanghaiChina Department of Obstetrics and Gynecology The Affiliated Suzhou Hospital of Nanjing Medical UniversitySuzhouJiangsu ProvinceChina

Intracerebral hemorrhage is a life-threatening condition with a high fatality rate and severe sequelae.However,there is currently no treatment available for intracerebral hemorrhage,unlike for other stroke subtypes.Recent studies have indicated that mitochondrial dysfunction and mitophagy likely relate to the pathophysiology of intracerebral hemorrhage.mitophagy,or selective autophagy of mitochondria,is an essential pathway to preserve mitochondrial homeostasis by clearing up damaged mitochondria.mitophagy markedly contributes to the reduction of secondary brain injury caused by mitochondrial dysfunction after intracerebral hemorrhage.This review provides an overview of the mitochondrial dysfunction that occurs after intracerebral hemorrhage and the underlying mechanisms regarding how mitophagy regulates it,and discusses the new direction of therapeutic strategies targeting mitophagy for intracerebral hemorrhage,aiming to determine the close connection between mitophagy and intracerebral hemorrhage and identify new therapies to modulate mitophagy after intracerebral hemorrhage.In conclusion,although only a small number of drugs modulating mitophagy in intracerebral hemorrhage have been found thus far,most of which are in the preclinical stage and require further investigation,mitophagy is still a very valid and promising therapeutic target for intracerebral hemorrhage in the long run.

关键词： intracerebral hemorrhage mitochondrial dysfunction mitophagy neuroinflammation neuroprotection reactive oxygen species secondary brain injury therapeutic target

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

mitophagy in neurodegenerative disease pathogenesis

引用

Neural Regeneration Research 2024年第5期19卷 998-1005页

作者： Kan Yang Yuqing Yan Anni Yu Ru Zhang Yuefang Zhang Zilong Qiu Zhengyi Li Qianlong Zhang Shihao Wu Fei Li Department of Developmental and Behavioural Pediatric&Child Primary Care Brain and Behavioural Research Unit of Shanghai Institute for Pediatric Research and MOE-Shanghai Key Laboratory for Children’s Environmental HealthXinhua HospitalShanghai Jiao Tong University School of MedicineShanghaiChina Center for Excellence in Brain Science and Intelligence Technology Institute of NeuroscienceState Key Laboratory of NeuroscienceCAS Key Laboratory of Primate NeurobiologyChinese Academy of SciencesShanghaiChina College of Materials and Chemical Engineering Hunan Institute of EngineeringXiangtanHunan ProvinceChina School of Medicine Yunnan UniversityKunmingYunnan ProvinceChina Songjiang Research Institute Shanghai Jiao Tong University School of MedicineShanghaiChina Neurosurgery Department Kunming Yenan HospitalKunmingYunnan ProvinceChina

Mitochondria are critical cellular energy resources and are central to the life of the neuron.mitophagy selectively clears damaged or dysfunctional mitochondria through autophagic machinery to maintain mitochondrial quality control and homeostasis.Mature neurons are postmitotic and consume substantial energy,thus require highly efficient mitophagy pathways to turn over damaged or dysfunctional mitochondria.Recent evidence indicates that mitophagy is pivotal to the pathogenesis of neurological diseases.However,more work is needed to study mitophagy pathway components as potential therapeutic targets.In this review,we briefly discuss the characteristics of nonselective autophagy and selective autophagy,including ERphagy,aggrephagy,and mitophagy.We then introduce the mechanisms of Parkin-dependent and Parkin-independent mitophagy pathways under physiological conditions.Next,we summarize the diverse repertoire of mitochondrial membrane receptors and phospholipids that mediate mitophagy.Importantly,we review the critical role of mitophagy in the pathogenesis of neurodegenerative diseases including Alzheimer’s disease,Parkinson’s disease,and amyotrophic lateral sclerosis.Last,we discuss recent studies considering mitophagy as a potential therapeutic target for treating neurodegenerative diseases.Together,our review may provide novel views to better understand the roles of mitophagy in neurodegenerative disease pathogenesis.

关键词： Alzheimer’s disease amyotrophic lateral sclerosis autophagy mitochondria mitophagy mitophagy receptor Parkin Parkinson’s disease PINK1

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Choline dehydrogenase interacts with SQSTM1 to activate mitophagy and promote coelomocyte survival in Apostichopus japonicus following Vibrio splendidus infection

引用

动物学研究(英文) 2023年第5期44卷 905-918页

作者： Lian-Lian Sun Ying-Fen Dai Mei-Xiang You Cheng-Hua Li State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products Ningbo UniversityNingboZhejiang 315211China Laboratory for Marine Fisheries Science and Food Production Processes Qingdao National Laboratory for Marine Science and TechnologyQingdaoShandong 266071China

Previous studies have shown that Vibrio splendidus infection causes mitochondrial damage in Apostichopus japonicus coelomocytes,leading to the production of excessive reactive oxygen species(ROS)and irreversible apoptotic cell death.Emerging evidence suggests that mitochondrial autophagy(mitophagy)is the most effective method for eliminating damaged mitochondria and ROS,with choline dehydrogenase(CHDH)identified as a novel mitophagy receptor that can recognize non-ubiquitin damage signals and microtubule-associated protein 1 light chain 3(LC3)in vertebrates.However,the functional role of CHDH in invertebrates is largely unknown.In this study,we observed a significant increase in the mRNA and protein expression levels of A.japonicus CHDH(AjCHDH)in response to V.splendidus infection and lipopolysaccharide(LPS)challenge,consistent with changes in mitophagy under the same conditions.Notably,AjCHDH was localized to the mitochondria rather than the cytosol following V.splendidus infection.Moreover,AjCHDH knockdown using si RNA transfection significantly reduced mitophagy levels,as observed through transmission electron microscopy and confocal microscopy.Further investigation into the molecular mechanisms underlying CHDH-regulated mitophagy showed that AjCHDH lacked an LC3-interacting region(LIR)for direct binding to LC3 but possessed a FB1 structural domain that binds to SQSTM1.The interaction between AjCHDH and SQSTM1 was further confirmed by immunoprecipitation analysis.Furthermore,laser confocal microscopy indicated that SQSTM1 and LC3 were recruited by AjCHDH in coelomocytes and HEK293T cells.In contrast,AjCHDH interference hindered SQSTM1 and LC3 recruitment to the mitochondria,a critical step in damaged mitochondrial degradation.Thus,AjCHDH interference led to a significant increase in both mitochondrial and intracellular ROS,followed by increased apoptosis and decreased coelomocyte survival.Collectively,these findings indicate that AjCHDH-mediated mitophagy plays a crucial role in coelomocyte survival in A.japon

关键词： Choline dehydrogenase mitophagy SQSTM1 Microtubule-associated protein 1 light chain 3 Apostichopus japonicus

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：