首站-论文投稿智能助手
典型文献
SARM1 participates in axonal degeneration and mitochondrial dysfunction in prion disease
文献摘要:
Prion disease represents a group of fatal neurogenerative diseases in humans and animals that are associated with energy loss, axonal degeneration, and mitochondrial dysfunction. Axonal degeneration is an early hallmark of neurodegeneration and is triggered by SARM1. We found that depletion or dysfunctional mutation of SARM1 protected against NAD+ loss, axonal degeneration, and mitochondrial functional disorder induced by the neurotoxic peptide PrP106–126. NAD+ supplementation rescued prion-triggered axonal degeneration and mitochondrial dysfunction and SARM1 overexpression suppressed this protective effect. NAD+ supplementation in PrP106–126-incubated N2a cells, SARM1 depletion, and SARM1 dysfunctional mutation each blocked neuronal apoptosis and increased cell survival. Our results indicate that the axonal degeneration and mitochondrial dysfunction triggered by PrP106–126 are partially dependent on SARM1 NADase activity. This pathway has potential as a therapeutic target in the early stages of prion disease.
文献关键词:
作者姓名:
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
作者机构:
National Animal Transmissible Spongiform Encephalopathy Laboratory,College of Veterinary Medicine,China Agricultural University,Beijing,China
引用格式:
[1]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-.SARM1 participates in axonal degeneration and mitochondrial dysfunction in prion disease)[J].中国神经再生研究(英文版),2022(10):2293-2299
A类:
SARM1,neurogenerative,Axonal,PrP106,NADase
B类:
participates,axonal,mitochondrial,prion,Prion,represents,group,fatal,diseases,humans,animals,that,are,associated,energy,loss,early,hallmark,neurodegeneration,triggered,by,We,found,depletion,dysfunctional,mutation,protected,against,NAD+,disorder,induced,neurotoxic,peptide,supplementation,rescued,overexpression,suppressed,this,protective,effect,incubated,N2a,cells,each,blocked,neuronal,apoptosis,increased,survival,Our,results,indicate,partially,dependent,activity,This,pathway,has,potential,therapeutic,target,stages
AB值:
0.436838
相似文献
Spirulina platensis aqueous extracts ameliorate colonic mucosal damage and modulate gut microbiota disorder in mice with ulcerative colitis by inhibiting inflammation and oxidative stress
Jian WANG;Liqian SU;Lun ZHANG;Jiali ZENG;Qingru CHEN;Rui DENG;Ziyan WANG;Weidong KUANG;Xiaobao JIN;Shuiqing GUI;Yinghua XU;Xuemei LU-Guangdong Provincial Key Laboratory of Pharmaceutical Bioactive Substances,School of Life Science and Biopharmaceutics,Guangdong Pharmaceutical University,Guangzhou 510006,China;School of Pharmacy,Guangdong Pharmaceutical University,Guangzhou 510006,China;Intensive Care Unit,Shenzhen Second People's Hospital,the First Affiliated Hospital of Shenzhen University,Shenzhen 518031,China;Key Laboratory of the Ministry of Health for Research on Quality and Standardization of Biotech Products,National Institutes for Food and Drug Control,Beijing 102629,China
TRDMT1 exhibited protective effects against LPS - induced inflammation in rats through TLR4- NF- κB / MAPK- TNF - α pathway
Zhengguang Li;Xiaolong Qi;Xu Zhang;Lei Yu;Lijuan Gao;Weining Kong;Wei Chen;Wei Dong;Lijun Luo;Dan Lu;Lianfeng Zhang;Yuanwu Ma-Key Laboratory of Human Disease Comparative Medicine,National Health Commission of China(NHC),Institute of Laboratory Animal Science,Chinese Academy of Medical Sciences,Peking Union Medicine College,Beijing,China;National Human Diseases Animal Model Resource Center and Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases,Institute of Laboratory Animal Science,Peking Union Medicine College,Chinese Academy of Medical Sciences,Beijing,China;Neuroscience Center,Chinese Academy of Medical Sciences,Beijing,China
CHCHD2 maintains mitochondrial contact site and cristae organizing system stability and protects against mitochondrial dysfunction in an experimental model of Parkinson’s disease
Lu Lin;Mao Hengxu;Zhou Miaomiao;Lin Yuwan;Dai Wei;Qiu Jiewen;Xiao Yousheng;Mo Mingshu;Zhu Xiaoqin;Wu Zhuohua;Pei Zhong;Guo Wenyuan;Xu Pingyi;Chen Xiang-Department of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510120, China;Department of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China;School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong 511436, China;Department of Neurology, National Key Clinical Department and Key Discipline of Neurology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, China
Astaxanthine attenuates cisplatin ototoxicity in vitro and protects against cisplatin-induced hearing loss in vivo
Benyu Nan;Zirui Zhao;Kanglun Jiang;Xi Gu;Huawei Li;Xinsheng Huang-Department of Otorhinolaryngology-Head and Neck Surgery,Zhongshan Hospital,Fudan University,Shanghai 200030,China;Department of Otorhinolaryngology-Head and Neck Surgery,Wenzhou Medical University,Affiliated Hospital 2,Wenzhou 325000,China;Department of Otolaryngology,Yueyang Hospital of Integrated Traditional Chinese and Western Medicine,Shanghai University of Traditional Chinese Medicine,Shanghai 200437,China;Department of Otolaryngology,the First Affiliated Hospital of Fujian Medical University,Fuzhou 350005,China;ENT Institute and Department of Otorhinolaryngology,Eye & ENT Hospital,State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science,Fudan University,Shanghai 200031,China;Institutes of Biomedical Sciences,Fudan University,Shanghai 200032,China;NHC Key Laboratory of Hearing Medicine(Fudan University),Shanghai 200031,China;The Institutes of Brain Science and the Collaborative Innovation Center for Brain Science,Fudan University,Shanghai 200032,China
Quantitative proteomics revealed extensive microenvironmental changes after stem cell transplantation in ischemic stroke
Yao Chen;Fahuan Song;Mengjiao Tu;Shuang Wu;Xiao He;Hao Liu;Caiyun Xu;Kai Zhang;Yuankai Zhu;Rui Zhou;Chentao Jin;Ping Wang;Hong Zhang;Mei Tian-Department of Nuclear Medicine and Medical PET Center,The Second Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310009,China;Institute of Nuclear Medicine and Molecular Imaging,Zhejiang University,Hangzhou 310009,China;Key Laboratory of Medical Molecular Imaging of Zhejiang Province,Hangzhou 310009,China;Department of Radiology,Zhejiang Hospital,Hangzhou 310030,China;Department of PET Center The First Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310006,China;Key Laboratory for Biomedical Engineering of Ministry of Education,Zhejiang University,Hangzhou 310027,China;College of Biomedical Engineering and Instrument Science,Zhejiang University,Hangzhou 310027,China;Shanxi Medical University,Taiyuan 030001,China
Mitochondrial aldehyde dehydrogenase(ALDH2)rescues cardiac contractile dysfunction in an APP/PS1 murine model of Alzheimer's disease via inhibition of ACSL4-dependent ferroptosis
Zhi-yun Zhu;Yan-dong Liu;Yan Gong;Wei Jin;Elena Topchiy;Subat Turdi;Yue-feng Gao;Bruce Culver;Shu-yi Wang;Wei Ge;Wen-liang Zha;Jun Ren;Zhao-hui Pei;Xing Qin-Jiangxi Provincial People's Hospital Affiliated to Nanchang University,Nanchang 330006,China;The Second Department of Cardiology,The Third Hospital of Nanchang,Nanchang 330009,China;University of Wyoming College of Health Sciences,Laramie,WY,USA;State Key Laboratory of Animal Nutrition,College of Animal Science and Technology,China Agricultural University,Beijing 100083,China;Department of General Practice,Xijing Hospital,the Air Force Military Medical University,Xi'an 710032,China;Department of Surgery,Clinic Medical College,Hubei University of Science and Technology,Xianning 437100,China;National Demonstration Center for Experimental General Medicine Education,Hubei University of Science and Technology,Xianning 437100,China;Department of Cardiology and Shanghai Institute of Cardiovascular Diseases,Zhongshan Hospital Fudan University,Shanghai 200032,China;Department of Cardiology,Xijing Hospital,the Air Force Military Medical University,Xi'an 710032,China
Corynoxine B derivative CB6 prevents Parkinsonian toxicity in mice by inducing PIK3C3 complex-dependent autophagy
Zhou Zhu;Liang-feng Liu;Cheng-fu Su;Jia Liu;Benjamin Chun-Kit Tong;Ashok lyaswamy;Senthilkumar Krishnamoorthi;Sravan Gopalkrishnashetty Sreenivasmurthy;Xin-jie Guan;Yu-xuan Kan;Wen-jian Xie;Chen-liang Zhao;King-ho Cheung;Jia-hong Lu;Jie-qiong Tan;Hong-jie Zhang;Ju-xian Song;Min Li-Mr.&Mrs.Ko Chi-Ming Centre for Parkinson's Disease Research,School of Chinese Medicine,Hong Kong Baptist University,Hong Kong,SAR,China;School of Chinese Medicine,Hong Kong Baptist University,Hong Kong,SAR,China;institute for Research and Continuing Education,Hong Kong Baptist University,Shenzhen 518057,China;Limin Pharmaceutical Factory,Livzon Group Limited,Shaoguan 512028,China;State Key Laboratory of Quality Research in Chinese Medicine,Institute of Chinese Medical Sciences,University of Macau,Macau,SAR,China;Center for Medical Genetics and Hunan Key Laboratory of Animal Model for Human Diseases,School of Life Sciences,Central South University,Changsha 410078,China;Medical College of Acupuncture-Moxibustion and Rehabilitation,Guangzhou University of Chinese Medicine,Guangzhou 510006,China
机标中图分类号,由域田数据科技根据网络公开资料自动分析生成,仅供学习研究参考。