详情页 - 聚合机构库演示平台

当前位置：首页 > 详情页

GENETIC ABLATION OF P65 SUBUNIT OF NF-kappa B IN MDX MICE TO IMPROVE MUSCLE PHYSIOLOGICAL FUNCTION

32| 认领 | 导出 | 链接全文 |

文献详情

资源类型：

WOS体系：

Pubmed体系：

收录情况： ◇ SCIE

作者：

单位： [1]Department of Orthopaedic Surgery, University of Pittsburgh, Suite 216, Bridgeside Point II, 450 Technology Drive, Pittsburgh, Pennsylvania, 15219 USA [2]Department of Geriatric Neurology, Chinese PLA General Hospital, Beijing, China [3]Beijing Friendship Hospital, Capital Medical University, Beijing, China

出处：

DOI：

ISSN：

关键词： DMD human dystrophin transgenic mice muscle physiological function NF-kappa B/p65 knockout mice NF-kappa B pathway

摘要：

Introduction: Duchenne muscular dystrophy (DMD) is a genetic muscle disease characterized by dystrophin deficiency. Beyond gene replacement, the question of whether ablation of the p65 gene of nuclear factor-kappa B (NF-kappa B) in DMD can improve muscle physiology function is unknown. In this study, we investigated muscle physiological improvement in mdx mice (DMD model) with a genetic reduction of NF-kappa B. Methods: Muscle physiological function and histology were studied in 2-month-old mdx/p65(+/-), wild-type, mdx, and human minidystrophin gene transgenic mdx (Tgh Delta Dys/mdx) mice. Results: Improved muscle physiological function was found in mdx/p65(+/-) mice when compared with mdx mice; however, it was similar to Tgh Delta Dys/mdx mice. The results indicate that genetic reduction of p65 levels diminished chronic inflammation in dystrophic muscle, thus leading to amelioration of muscle pathology and improved muscle physiological function. Conclusions: The results show that inhibition of NF-kappa B may be a promising therapy when combined with gene therapy for DMD.

基金：

语种：

被引次数：

WOS：

PubmedID：

中科院(CAS)分区：

出版当年[2016]版：

大类 | 3 区医学

小类 | 3 区临床神经病学 4 区神经科学

最新[2025]版：

大类 | 3 区医学

小类 | 3 区临床神经病学 3 区神经科学

JCR分区：

出版当年[2015]版：

Q2 NEUROSCIENCES Q2 CLINICAL NEUROLOGY

最新[2023]版：

Q2 CLINICAL NEUROLOGY Q2 NEUROSCIENCES

影响因子： 最新[2023版] 2.8 最新五年平均[2021-2025] 3.1 出版当年[2015版] 2.713 出版当年五年平均[2011-2015] 2.474 出版前一年[2014版] 2.283 出版后一年[2016版] 2.605

第一作者：

第一作者单位： [1]Department of Orthopaedic Surgery, University of Pittsburgh, Suite 216, Bridgeside Point II, 450 Technology Drive, Pittsburgh, Pennsylvania, 15219 USA [2]Department of Geriatric Neurology, Chinese PLA General Hospital, Beijing, China

通讯作者：

推荐引用方式(GB/T 7714)：

APA：

MLA：

相关文献

[1]Berberine Ameliorates Subarachnoid Hemorrhage InjuryviaInduction of Sirtuin 1 and Inhibiting HMGB1/Nf-kappa B Pathway [2]Protective effect of alpha-pinene against isoproterenol-induced myocardial infarction through NF-kappa B signaling pathway [3]TRIB3 alters endoplasmic reticulum stress-induced beta-cell apoptosis via the NF-kappa B pathway [4]Liraglutide inhibited AGEs induced coronary smooth muscle cell phenotypic transition through inhibiting the NF-kappa B signal pathway [5]TRIM9 overexpression promotes uterine leiomyoma cell proliferation and inhibits cell apoptosis via NF-kappa B signaling pathway [6]Dapk1 improves inflammation, oxidative stress and autophagy in LPS-induced acute lung injury via p38MAPK/NF-kappa B signaling pathway [7]CXCL5 promotes mitomycin C resistance in non-muscle invasive bladder cancer by activating EMT and NF-kappa B pathway [8]Cyclooxygenase 2 promotes proliferation and invasion in ovarian cancer cells via the PGE2/NF-kappa B pathway [9]Inflammatory response is modulated by lincRNACox2 via the NF-kappa B pathway in macrophages infected by Mycobacterium tuberculosis [10]Bisabolol attenuates sepsis-induced acute lung injury through inhibiting NF-kappa B-mediated inflammatory response