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中国药理学与毒理学杂志 2019年第10期 841-842页

作者： BAI Xue DU Xiao HE Xiao-li Institute of Medicinal Plant Development Chinese Academy of Medical Sciences and Peking Union Medical College

OBJECTIVE To explore the effect of the active components group of Xiaoxuming decoction(XXMD)on mitophagy after cerebral ischemia/reperfusion(I/R) in MCAO rats. METHODS Male Sprague-Dawley rats were randomly divided into 4 groups: sham group, XXMD and rapamycin group. The I/R models were induced by middle cerebral artery occlusion. The effects of XXMD and rapamycin on behavioral study of focal cerebral I/R in rats were measured by Zea-Longa′ s level standard scoring method and neurological defect score(m NSS). The volume percentage and hemispheric swelling of rat cerebral infarction were detected by TTC staining. Proteins in the mitophagy were detected by Western blotting. RESULTS The behavioral results showed that compared with the model group, XXMD decoction and rapamycin could significantly alleviate the neurological deficit scores after I/R, decreased the m NSS score(Pmitophagy were activated at 24 h after cerebral I/R, and then it was inhibited. XXMD can protect mitochondrial structures, regulate the level of mitophagy at different points after cerebral I/R, inhibit the excessive activation of mitophagy in 24 h after I/R, and improve the level of mitophagy in the later stage of I/R.

关键词： active components Xiaoxuming decoction cerebral ischemic reperfusion mitochondrial function mitophagy

mitophagy in the Skeletal Muscle Is Suppressed in Spleen Qi Deficiency

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Chinese Medicine 2019年第1期10卷 11-18页

作者： Dan Ma Wenjun Liu Lu Wang Xinzhu Xu Lingzhi Wang Huaxin Yu Xudong Liu Huihui Liu Deshan Wang Dehong Shan School of Basic Medicine Liaoning University of Traditional Chinese Medicine Shenyang China Teaching and Experimental Center Liaoning University of Traditional Chinese Medicine Shenyang China

Objective: Mitochondrial impairment in the skeletal muscle contributes to useless of limbs in spleen qi deficiency;however the genesis of such impairment is not clear. Herein, PTEN-induced putative kinase 1 (PINK1)-Parkin pathway and mitophagy were studied to explore the machinery of mitochondrial impairment. Methods: 16 male SD rats were randomly divided in the control group and spleen qi deficiency group (model group);transmission electron microscope was used to observe mitochondrial morphology;mitochondrial oxidative phosphorylation was assessed by testing mitochondrial membrane potential (MMP) and levels of ATP and ROS;western blot was used to analyze expressions of PINK1, Parkin, microtubule-associated protein 1 light chain 3-II (LC3-II) and p62. Results: Compared with those in the control group, mitochondria became small, less and scattered, MMP and the ATP level were reduced, the ROS level was elevated, PINK1 expression was decreased, p62 expression was increased, but Parkin and LC3-II expressions were not altered, in the model group. Conclusions: Suppression of mitophagy might be related to the mitochondrial damage in the skeletal muscle when spleen qi deficiency develops.

关键词： Spleen Qi Deficiency mitophagy PINK1 Parkin LC3 p62 Muscle

mitophagy is induced by PTEN-induced kinase 1 gene silencing in dopaminergic neurons

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Mitophagy is induced by PTEN-induced kinase 1 gene silencing...

Hepatitis B virus core protein as a Rab-GAP suppressor driving liver disease progression

中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Zhi-Feng Qi,Tao CUI,Li LV,Hua GAO,Hui YANG~* Beijing Institute for Neuroscience,Capital Medical University,Beijing Center for Neural Regeneration & Repair,Key Laboratory for Neurodegenerative Disease of the Ministry of Education,Beijing 100069,China

＜正＞Parkinson’s disease is a common neurodegenerative *** studies indicate that the abnormal autophagy in neurons is the main reason for the generation of ***1（PTEN-induced kinase 1） is one of PD-related genes, which is directly involved in the 1 function of ***,it is not clear that autophagy could be activated by mitochondrial injury induced by PINK1 gene *** study showed that silencing PINK1 may induce autophagy in dopaminegic cell line（MN9D）.We found that the level of LC3II（vacuole membrane associate type）,which has been accepted as marker of autophagy,increased significantly at 48h since PINK1 silencing by Western *** number of vacuoles with mitochondria,which are enclosed by double membrane（mitophagy） was also observed to increase in the group of PINK1 RNA *** of monodansylcadaverine（MDC） and acidotropic orange staining also showed that the level of autophagy was induced significantly by PINK1 gene ***,the level of Beclinl and phosphorylation of Bcl2（p-Bcl2） were increased and the generation of reactive oxygen species（ROS） was also elevated when silencing PINK1 gene in *** conclusion,our study suggests that PINK1 gene silencing may increase the ROS generation and induce mitophagy by activating Beclinl and p-Bcl2 and may provide a clue to find new drugs for the treatment of PD in clinic.

关键词： PINK1 mitophagy Bcl-2 RNA interference Parkinson’s disease.

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Science Bulletin 2024年第16期69卷 2580-2595页

作者： Yu Su Fan Bu Yuanfei Zhu Le Yang Qiong Wu Yuan Zheng Jianjin Zhao Lin Yu Nan Jiang Yongxiang Wang Jian Wu Youhua Xie Xinxin Zhang Yueqiu Gao Ke Lan Qiang Deng Key Laboratory of Medical Molecular Virology(MOE/NHC/CAMS) School of Basic Medical SciencesShanghai Institute of Infectious Disease and BiosecurityFudan UniversityShanghai 200032China Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection Fudan UniversityShanghai 200032China Department of Infectious Diseases Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China Laboratory of Cellular Immunity Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese MedicineShanghai 201203China State Key Laboratory of Virology College of Life SciencesWuhan UniversityWuhan 430072China

Chronic hepatitis B virus(HBV)infection can lead to advanced liver ***,we establish a transgenic murine model expressing a basic core promoter(BCP)-mutated HBV *** previous studies on the wild-type virus,the BCP-mutated HBV transgenic mice manifest chronic liver injury that culminates in cirrhosis and tumor development with ***,agonistic anti-Fas treatment induces fulminant hepatitis in these mice even at a negligible *** the BCP mutant exhibits a striking increase in HBV core protein(HBc)expression,we posit that HBc is actively involved in hepatocellular ***,HBc interferes with Fis1-stimulated mitochondrial recruitment of Tre-2/Bub2/Cdc16 domain family member 15(TBC1D15).HBc may also inhibit multiple Rab GTPase-activating proteins,including Rab7-specific TBC1D15 and TBC1D5,by binding to their conserved catalytic *** cells under mitochondrial stress,HBc thus perturbs mitochondrial dynamics and prevents the recycling of damaged ***,sustained HBc expression causes lysosomal consumption via Rab7 hyperactivation,which further hampers late-stage autophagy and substantially increases apoptotic cell ***,we show that adenovirally expressed HBc in a mouse model is directly cytopathic and causes profound liver injury,independent of antigen-specific immune *** findings reveal an unexpected cytopathic role of HBc,making it a pivotal target for HBV-associated liver disease *** BCP-mutated HBV transgenic mice also provide a valuable model for understanding chronic hepatitis B progression and for the assessment of therapeutic strategies.

关键词： Apoptosis Basic core promoter mitophagy Rab7 Transgenic mice

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Selective Degradation of Mitochondria by mitophagy in Pathogenic Fungi

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American Journal of Molecular Biology 2021年第1期11卷 15-27页

作者： Jane Sadhna Jagernath Shuai Meng Jiehua Qiu Huanbin Shi Yanjun Kou State Key Laboratory of Rice Biology China National Rice Research Institute Hangzhou China

Selective mitochondrial autophagy or mitophagy is an evolutionarily conserved cellular process that selectively degrades superfluous, damaged, and dysfunctional mitochondria. This process is believed to be a mitochondrial quality control system crucial for intracellular homeostasis. Recently, researchers developed a range of methods to induce mitophagy and a variety of assays to monitor this process. With these new methods, the research on mitophagy has been developed rapidly. In particular, some key receptors and regulatory factors in fungi have been identified, which provides a basis for further understanding of the mechanism of this process. Although it has been studied extensively in the model yeast Saccharomyces cerevisiae, mitophagy in pathogenic fungi remains poorly understood. However recent studies have shown that mitophagy is involved in the regulation of pathogenicity of pathogenic fungi, which greatly increases the importance of mitophagy. Therefore, it is necessary to review the current research on mitophagy in order to provide an accurate understanding of mitophagy and promote mitophagy research in the pathogenic fungi.

关键词： Mitochondria mitophagy Yeast Pathogenic Fungi

Latest assessment methods for mitochondrial homeostasis in cognitive diseases

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Neural Regeneration Research 2024年第4期19卷 754-768页

作者： Wei You Yue Li Kaixi Liu Xinning Mi Yitong Li Xiangyang Guo Zhengqian Li Department of Anesthesiology Peking University Third Hospital Peking University Third Clinical Medical College Beijing Center of Quality Control and Improvement on Clinical Anesthesia Anesthesia and Perioperative Medicine Branch of China International Exchange and Promotive Association for Medical and Health Care(CPAM)

Mitochondria play an essential role in neural function,such as supporting normal energy metabolism,regulating reactive oxygen species,buffering physiological calcium loads,and maintaining the balance of morphology,subcellular distribution,and overall health through mitochondrial *** the recent technological advances in the assessment of mitochondrial structure and functions,mitochondrial dysfunction has been regarded as the early and key pathophysiological mechanism of cognitive disorders such as Alzheimer’s disease,Parkinson’s disease,Huntington’s disease,mild cognitive impairment,and postoperative cognitive *** review will focus on the recent advances in mitochondrial medicine and research methodology in the field of cognitive sciences,from the perspectives of energy metabolism,oxidative stress,calcium homeostasis,and mitochondrial dynamics(including fission-fusion,transport,and mitophagy).

关键词： cognitive disorders mitochondrial dysfunction mitochondrial energy metabolism mitochondrial dynamics mitochondrial transport mitophagy mitochondrial biogenesis oxidative stress calcium homeostasis

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Hernandezine promotes cancer cell apoptosis and disrupts the lysosomal acidic environment and cathepsin D maturation

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Chinese Journal of Natural Medicines 2024年第5期22卷 387-401页

作者： FENG Qianwen SUN Lu Muhammad Jibran Sualeh ZHAO Qingli ZHAO Songji CUI Zhengguo INADERA Hidekuni Department of Public Health Graduate School of Medicine and Pharmaceutical SciencesUniversity of ToyamaToyama 930-8501Japan Department of Pediatric Cardiology Heart CenterGuangzhou Women and Children’s Medical CenterGuangzhou Medical UniversityGuangzhou 510000China Department of Basic Medical Sciences College of MedicineUniversity of SharjahSharjah 57545United Arab Emirates Department of Radiology Graduate School of Medicine and Pharmaceutical SciencesUniversity of ToyamaToyama 930-8501Japan Advanced Clinical Research Center Fukushima Global Medical Science CenterFukushima Medical UniversityFukushima CityFukushima 960-8074Japan Department of Environmental Health School of Medical SciencesUniversity of FukuiFukui 910-8580Japan

Hernandezine(Her),a bisbenzylisoquinoline alkaloid extracted from Thalictrum flavum,is recognized for its range of biological activities inherent to this herbal *** its notable properties,the anti-cancer effects of Her have remained largely *** this study,we elucidated that Her significantly induced cytotoxicity in cancer cells through the activation of apoptosis and necroptosis ***,Her triggered autophagosome formation by activating the AMPK and ATG5 conjugation systems,leading to LC3 *** findings revealed that Her caused damage to the mitochondrial membrane,with the damaged mitochondria undergoing mitophagy,as evidenced by the elevated expression of mitophagy ***,Her disrupted autophagic flux,demonstrated by the upregulation of p62 and accumulation of autolysosomes,as observed in the RFP-GFP-LC3 reporter ***,we determined that Her did not prevent the fusion of autophagosomes and ***,it inhibited the maturation of cathepsin D and increased lysosomal pH,indicating an impairment of lysosomal *** use of the early-stage autophagy inhibitor,3-methyladenine(3-MA),did not suppress LC3II,suggesting that Her also induces noncanonical autophagy in autophagosome *** application of Bafilomycin A1,an inhibitor of noncanonical autophagy,diminished the recruitment of ATG16L1 and the accumulation of LC3II by Her,thereby augmenting Her-induced cell *** observations imply that while autophagy initially plays a protective role,the disruption of the autophagic process by Her promotes programmed cell *** study provides the first evidence of Her’s dual role in inducing apoptosis and necroptosis while also initiating and subsequently impairing autophagy to promote apoptotic cell *** insights contribute to a deeper understanding of the mechanisms underlying programmed cell death,offering potential avenues for enhancing cancer prevention and therapeutic st

关键词： Hernandezine Apoptosis mitophagy Autophagic flux Lysosome Noncanonical autophagy

Alginate oligosaccharide-mediated butyrate-HIF-1a axis improves skin aging in mice

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Journal of Pharmaceutical Analysis 2024年第5期14卷 678-692页

作者： Ting Gao Yixuan Li Xiaoyu Wang Fazheng Ren Department of Nutrition and Health College of Veterinary MedicineChina Agricultural UniversityBeijing100083China

The“gut-skin”axis has been proved and is considered as a novel therapy for the prevention of skin *** antioxidant efficacy of oligomannonic acid(MAOS)makes it an intriguing target for use to improve skin *** present study further explored whereby MAOS-mediated gut-skin axis balance prevented skin aging in *** data indicated the skin aging phenotypes,oxidative stress,skin mitochondrial dysfunction,and intestinal dysbiosis(especially the butyrate and HIF-1a levels decreased)in aging ***,fecal microbiota transplantation(FMT)from aging mice rebuild the aging-like ***,we demonstrated MAOS-mediated colonic butyrate-HIF-1a axis homeostasis promoted the entry of butyrate into the skin,upregulated mitophagy level and ultimately improving skin aging via HDAC3/PHD/HIF-1a/mitophagy loop in skin of ***,our study offered a better insights of the effectiveness of alginate oligosaccharides(AOS),promised to become a personalized targeted therapeutic agents,on gut-skin axis disorder inducing skin aging.

关键词： Alginate oligosaccharide Skin aging Butyrate HIF-1a mitophagy

Molecular regulation of receptor-mediated mitophagy

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Molecular regulation of receptor-mediated mitophagy

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

中国生物化学与分子生物学会2016年全国学术会议

作者： Quan Chen Institute of Zoology Chinese Academy of Sciences

Mitochondria control both the life and death of a *** ensure the well-being of the cell,mitochondrial quality and quantity is tightly monitored through a mechanism called mitophagy,which selectively removes damaged or unwanted *** recently identified that the mitochondrial outer membrane protein FUNDC1 harbors a LC3-interacting region(LIR)and interacts with LC3 to mediate mitophagy

关键词： mitophagy FUNDC1 Mitochondrial quality control

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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

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