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Novel nervous and multi-system regenerative therapeutic strategies for diabetes mellitus with mTOR 被引量:13
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作者 Kenneth Maiese 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第3期372-385,共14页
Throughout the globe,diabetes mellitus(DM) is increasing in incidence with limited therapies presently available to prevent or resolve the significant complications of this disorder.DM impacts multiple organs and af... Throughout the globe,diabetes mellitus(DM) is increasing in incidence with limited therapies presently available to prevent or resolve the significant complications of this disorder.DM impacts multiple organs and affects all components of the central and peripheral nervous systems that can range from dementia to diabetic neuropathy.The mechanistic target of rapamycin(m TOR) is a promising agent for the development of novel regenerative strategies for the treatment of DM.m TOR and its related signaling pathways impact multiple metabolic parameters that include cellular metabolic homeostasis,insulin resistance,insulin secretion,stem cell proliferation and differentiation,pancreatic β-cell function,and programmed cell death with apoptosis and autophagy.m TOR is central element for the protein complexes m TOR Complex 1(m TORC1) and m TOR Complex 2(m TORC2) and is a critical component for a number of signaling pathways that involve phosphoinositide 3-kinase(PI 3-K),protein kinase B(Akt),AMP activated protein kinase(AMPK),silent mating type information regulation 2 homolog 1(Saccharomyces cerevisiae)(SIRT1),Wnt1 inducible signaling pathway protein 1(WISP1),and growth factors.As a result,m TOR represents an exciting target to offer new clinical avenues for the treatment of DM and the complications of this disease.Future studies directed to elucidate the delicate balance m TOR holds over cellular metabolism and the impact of its broad signaling pathways should foster the translation of these targets into effective clinical regimens for DM. 展开更多
关键词 Akt AMP activated protein kinase(AMPK) apoptosis Alzheimer’s disease autophagy β-cell cancer cardiovascular disease caspase CCN family diabetes mellitus epidermal growth factor erythropoietin fibroblast growth factor forkhead transcription factors Fox O frap1 hamartin(tuberous sclerosis 1)/tuberin(tuberous sclerosis 2)(TSC1/TSC2) insulin mechanistic target of rapamycin(mTOR) m TOR Complex 1(m T ORC1) m TOR Complex 2(m TORC2) nicotinamide nicotinamide adenine dinucleotide(NAD+) non-communicable diseases oxidative stress phosphoinositide 3-kinase(PI 3-K) programmed cell death silent mating type information regulation 2 homolog 1(Saccharomyces cerevisiae)(SIRT1) sirtuin stem cells wingless Wnt Wnt1 inducible signaling pathway protein 1(WISP1)
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戒断综合征的治疗靶点
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作者 阿明 《国外医学情报》 2002年第11期13-13,共1页
人们都知道,如果清晨没有喝那杯不可缺少的咖啡,就会变得非常易怒。同样,癌细胞也会对刺激物成瘾。在近期出版的《国家科学院进展》杂志上发表的两篇文章揭示说,具有极度活性的磷脂酰肌醇3-激酶(PL3K)通路的癌细胞依赖它来激活FRAP1(mTO... 人们都知道,如果清晨没有喝那杯不可缺少的咖啡,就会变得非常易怒。同样,癌细胞也会对刺激物成瘾。在近期出版的《国家科学院进展》杂志上发表的两篇文章揭示说,具有极度活性的磷脂酰肌醇3-激酶(PL3K)通路的癌细胞依赖它来激活FRAP1(mTOR),后者能调节核糖体的生成。这使得这些细胞对Rapamisin更敏感。目前,Rapamisin已经作为免疫抑制剂上市销售。 展开更多
关键词 frap1 磷脂酰肌醇3-激酶 治疗靶点 戒断综合征
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