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肥胖与衰老的分子联系:聚焦于脂肪蛋白53和视网膜母细胞瘤蛋白。

Molecular connections of obesity and aging: a focus on adipose protein 53 and retinoblastoma protein.

作者信息

Chu Dinh-Toi, Tao Yang

机构信息

Institute for Research and Development, Duy Tan University, K7/25 Quang Trung, Danang, Vietnam.

Faculty of Biology, Hanoi National University of Education, Hanoi, Vietnam.

出版信息

Biogerontology. 2017 Jun;18(3):321-332. doi: 10.1007/s10522-017-9698-4. Epub 2017 Mar 30.

DOI:10.1007/s10522-017-9698-4
PMID:28357524
Abstract

Obesity is an induced health problem that human beings have been facing with non-optimal treatment so far. Humans are on average getting fatter with age, and obesity and aging interact each other to shorten lifetime and decrease life quality. Obesity also causes several aging related-disorders such as cancer, strokes, cardiovascular disease, high blood pressure and type 2 diabetes. So, the molecular connections between aging and obesity are promising targets for bio-medical researches and innovative therapies of many health problems. In this review, we discuss the findings of adipose p53 and Rb-two central molecular linkages between aging and obesity-on lipid metabolism and obesity.

摘要

肥胖是一个人为导致的健康问题,到目前为止人类一直面临着非最佳治疗方法。随着年龄增长,人类平均变得越来越胖,肥胖与衰老相互作用,缩短寿命并降低生活质量。肥胖还会引发多种与衰老相关的疾病,如癌症、中风、心血管疾病、高血压和2型糖尿病。因此,衰老与肥胖之间的分子联系是生物医学研究和许多健康问题创新疗法的有前景的靶点。在这篇综述中,我们讨论脂肪组织中的p53和Rb——衰老与肥胖之间两个核心分子联系——对脂质代谢和肥胖的研究结果。

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1
Molecular connections of obesity and aging: a focus on adipose protein 53 and retinoblastoma protein.肥胖与衰老的分子联系:聚焦于脂肪蛋白53和视网膜母细胞瘤蛋白。
Biogerontology. 2017 Jun;18(3):321-332. doi: 10.1007/s10522-017-9698-4. Epub 2017 Mar 30.
2
Deficiency in p53 but not retinoblastoma induces the transformation of mesenchymal stem cells in vitro and initiates leiomyosarcoma in vivo.p53 缺失而非视网膜母细胞瘤导致间充质干细胞在体外转化,并在体内引发平滑肌肉瘤。
Cancer Res. 2010 May 15;70(10):4185-94. doi: 10.1158/0008-5472.CAN-09-4640. Epub 2010 May 4.
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[TP53 and RB tumor suppressor pathways collaborate in retinoblastoma genesis].[TP53与RB肿瘤抑制通路在视网膜母细胞瘤发生过程中协同作用]
Med Sci (Paris). 2007 Apr;23(4):356-8. doi: 10.1051/medsci/2007234356.
4
Tumour biology. p53, guardian of Rb.
Nature. 1994 Sep 1;371(6492):21-2. doi: 10.1038/371021a0.
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Human fibroblasts require the Rb family of tumor suppressors, but not p53, for PML-induced senescence.人成纤维细胞在PML诱导的衰老过程中需要肿瘤抑制因子Rb家族,但不需要p53。
Oncogene. 2004 Jan 8;23(1):91-9. doi: 10.1038/sj.onc.1206886.
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Haploinsufficiency of the retinoblastoma protein gene reduces diet-induced obesity, insulin resistance, and hepatosteatosis in mice.视网膜母细胞瘤蛋白基因的单倍剂量不足可减轻小鼠饮食诱导的肥胖、胰岛素抵抗和肝脂肪变性。
Am J Physiol Endocrinol Metab. 2009 Jul;297(1):E184-93. doi: 10.1152/ajpendo.00163.2009. Epub 2009 May 5.
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Partial proteasome inhibition in human fibroblasts triggers accelerated M1 senescence or M2 crisis depending on p53 and Rb status.人类成纤维细胞中的部分蛋白酶体抑制会根据p53和Rb状态引发加速的M1衰老或M2危机。
Aging Cell. 2008 Oct;7(5):717-32. doi: 10.1111/j.1474-9726.2008.00425.x. Epub 2008 Aug 1.
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Effect of tumor suppressors on cell cycle-regulatory genes: RB suppresses p34cdc2 expression and normal p53 suppresses cyclin A expression.肿瘤抑制因子对细胞周期调控基因的影响:RB抑制p34cdc2表达,正常p53抑制细胞周期蛋白A表达。
Exp Cell Res. 1994 Jan;210(1):94-101. doi: 10.1006/excr.1994.1014.
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Role of p53 and RB on in vitro growth of normal umbilical cord blood cells.p53和RB对正常脐带血细胞体外生长的作用。
Exp Hematol. 1996 May;24(6):702-12.
10
Emerging roles of RB family: new defense mechanisms against tumor progression.RB 家族的新兴作用:抵御肿瘤进展的新防御机制。
J Cell Physiol. 2013 Mar;228(3):525-35. doi: 10.1002/jcp.24170.

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