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Beta-asarone attenuates amyloid beta-induced autophagy via Akt/mTOR pathway in PC12 cells.β-细辛醚通过Akt/mTOR通路减轻PC12细胞中淀粉样蛋白β诱导的自噬。
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μ-Opioid receptor attenuates Aβ oligomers-induced neurotoxicity through mTOR signaling.μ-阿片受体通过mTOR信号通路减轻Aβ寡聚体诱导的神经毒性。
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CSF lactate levels, τ proteins, cognitive decline: a dynamic relationship in Alzheimer's disease.脑脊液乳酸水平、τ 蛋白、认知下降:阿尔茨海默病中的动态关系。
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Ex vivo protective effects of nicotinamide and 3-aminobenzamide on rat synaptosomes treated with Aβ(1-42).烟酰胺和3-氨基苯甲酰胺对用Aβ(1-42)处理的大鼠突触体的体外保护作用。
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Taking aim at Alzheimer's disease through the mammalian target of rapamycin.通过雷帕霉素的哺乳动物靶点针对阿尔茨海默病
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Erythropoietin priming improves the vasculogenic potential of G-CSF mobilized human peripheral blood mononuclear cells.促红细胞生成素预处理可提高 G-CSF 动员的人外周血单个核细胞的血管生成潜能。
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Low-dose PTH increases osteoblast activity via decreased Mef2c/Sost in senescent osteopenic mice.低剂量甲状旁腺激素通过降低衰老性骨质疏松小鼠的Mef2c/Sost来增加成骨细胞活性。
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WISP1:CCN 家族中具有促增殖和修复功能的成员的临床见解。

WISP1: Clinical insights for a proliferative and restorative member of the CCN family.

机构信息

Cellular and Molecular Signaling, Newark, New Jersey 07101, USA.

出版信息

Curr Neurovasc Res. 2014;11(4):378-89. doi: 10.2174/1567202611666140912115107.

DOI:10.2174/1567202611666140912115107
PMID:25219658
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4205162/
Abstract

As a proliferative and restorative entity, Wnt1 inducible signaling pathway protein 1 (WISP1) is emerging as a novel target for a number of therapeutic strategies that are relevant for disorders such as traumatic injury, neurodegeneration, musculoskeletal disorders, cardiovascular disease, pulmonary compromise, and control of tumor growth as well as distant metastases. WISP1, a target of the wingless pathway Wnt1, oversees cellular mechanisms that include apoptosis, autophagy, cellular migration, stem cell proliferation, angiogenesis, immune cell modulation, and tumorigenesis. The signal transduction pathways of WISP1 are broad and involve phosphoinositide 3-kinase (PI 3-K), protein kinase B (Akt), mitogen activated protein (MAP) kinase, c-Jun N-terminal kinase (JNK), caspases, forkhead transcription factors, sirtuins, c-myc, glycogen synthase kinase -3β (GSK-3β), β-catenin, miRNAs, and the mechanistic target of rapamaycin (mTOR). Ultimately, these signal transduction pathways of WISP1 can result in varied and sometimes unpredictable outcomes especially for cell survival, tissue repair, and tumorigenesis that demand increased insight into the critical role WISP1 holds for cellular biology and clinical medicine.

摘要

作为一种增殖和修复实体,Wnt1 诱导信号通路蛋白 1(WISP1)作为许多治疗策略的新靶点出现,这些治疗策略与创伤、神经退行性变、肌肉骨骼疾病、心血管疾病、肺损伤以及肿瘤生长和远处转移的控制等疾病有关。WISP1 是 Wnt1 通路的一个靶点,负责监督包括细胞凋亡、自噬、细胞迁移、干细胞增殖、血管生成、免疫细胞调节和肿瘤发生在内的细胞机制。WISP1 的信号转导途径广泛,涉及磷酸肌醇 3-激酶(PI3-K)、蛋白激酶 B(Akt)、丝裂原激活蛋白(MAP)激酶、c-Jun N 末端激酶(JNK)、半胱天冬酶、叉头转录因子、沉默调节蛋白、c-myc、糖原合酶激酶-3β(GSK-3β)、β-连环蛋白、miRNA 和雷帕霉素的机制靶点(mTOR)。最终,WISP1 的这些信号转导途径可能导致不同的、有时甚至不可预测的结果,尤其是对于细胞存活、组织修复和肿瘤发生,这需要深入了解 WISP1 在细胞生物学和临床医学中的关键作用。