title: Therapeutic effect of recombinant lentiviral vector containing succinate dehydrogenase iron-sulfur protein on the treatment of experimental autoimmunity myocarditis.
abstract: Cardiac autoimmune reaction takes part in myocarditis, dilated cardiomyopathy and heart failure. Existing literature has confirmed that the occurrence of cardiomyopathy belongs to mitochondrial diseases and is related to the oxidative respiratory chain subunit. The special structure of iron-sulfur protein (ISP) is responsible for the oxidative stress in oxidative phosphorylation, which is also a target that is easily attacked by various damage factors. Using gene therapy technology to restore succinate dehydrogenase iron-sulfur protein (SDISP) function- and thus resume myocardial mitochondria function and myocardial function is hypothesized to alleviate the experimental autoimmunity myocarditis (EAM).
authors.affiliation: Department of Cardiovascular Internal Medicine, Nanlou Branch of Chinese People's Liberation Army General Hospital, Beijing 100853, China.
authors.forename: Lina
authors.initials: L
authors.lastname: Han
authors.affiliation: Department of General Surgery, Chinese People's Liberation Army General Hospital, Beijing 100853, China.
authors.forename: Chunxi
authors.initials: C
authors.lastname: Wang
authors.affiliation: School of Automation, Beijing Institute of Technology, Beijing 100081, China. Electronic address: guoshuli@bit.edu.cn.
authors.forename: Shuli
authors.initials: S
authors.lastname: Guo
authors.affiliation: Medical Imaging, Harbin Medical University, Harbin 150000, China.
authors.forename: Siyu
authors.initials: S
authors.lastname: Liu
authors.affiliation: Department of Cardiac Surgery, First Bethune Hospital of Jilin University, Xinmin Street, Changchun, Jilin Province 130021, China.
authors.forename: Liming
authors.initials: L
authors.lastname: Yang
mesh_terms: D000818:Animals; D017209:Apoptosis; D001327:Autoimmune Diseases / Q000628:therapy*; D015551:Autoimmunity; D002311:Cardiomyopathy, Dilated / Q000628:therapy; D004195:Disease Models, Animal; D004452:Echocardiography; D004579:Electron Transport; D015316:Genetic Therapy; D005822:Genetic Vectors; D006333:Heart Failure / Q000628:therapy; D006439:Hemodynamics; D007249:Inflammation; D007506:Iron-Sulfur Proteins / Q000235:genetics / Q000627:therapeutic use*; D016086:Lentivirus / Q000235:genetics*; D008928:Mitochondria / Q000378:metabolism; D009205:Myocarditis / Q000628:therapy*; D010085:Oxidative Phosphorylation; D018384:Oxidative Stress; D051381:Rats; D011917:Rats, Inbred Lew; D013385:Succinate Dehydrogenase / Q000235:genetics / Q000627:therapeutic use*
chemical_list: D007506:Iron-Sulfur Proteins; D013385:Succinate Dehydrogenase