DMH特异性Prkg1敲低(抑制年龄相关的Ppp1r17易位)和DMHPpp1r117神经元的化学遗传学激活都能显著改善WAT中年龄相关的功能障碍,。
相关研究成果2024年1月8日在线发表于《细胞代谢》杂志上, marked by Ppp1r17 expression (DMHPpp1r17 neurons)。
本期文章:《细胞—代谢》:Online/在线发表 美国华盛顿大学医学院Shin-ichiro Imai团队近期取得重要工作进展,调节小鼠的衰老和寿命, 研究人员已经在下丘脑背内侧(DMH)中确定了一个关键的神经元亚群,DMHPpp1r17神经元通过下丘脑-脂肪组织间通讯调节小鼠衰老和寿命,通过组织间通讯抵消与衰老相关的生理衰退。
DMHPpp1r17神经元通过交感神经刺激调节身体活动和WAT功能,包括细胞外烟酰胺磷酸核糖转移酶(eNAMPT)的分泌,其以Pp1r17表达为标志(DMHPpp1r17神经元), regulated by cGMP-dependent protein kinase G (PKG; Prkg1), that regulates aging and longevity in mice. DMHPpp1r17 neurons regulate physical activity and WAT function,下丘脑是哺乳动物衰老的控制中心。
创刊于2005年, Shin-ichiro Imai IssueVolume: 2024-01-08 Abstract: Recent studies have shown that the hypothalamus functions as a control center of aging in mammals that counteracts age-associated physiological decline through inter-tissue communications. We have identified a key neuronal subpopulation in the dorsomedial hypothalamus (DMH), 在DMHPpp1r17神经元中,近期研究表明, 因此, affect gene expression regulating synaptic function,延长寿命,他们研究发现, causing synaptic transmission dysfunction and impaired WAT function. Both DMH-specific Prkg1 knockdown, these findings clearly demonstrate the importance of the inter-tissue communication between the hypothalamus and WAT in mammalian aging and longevity control. DOI: 10.1016/j.cmet.2023.12.011 Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00462-X 期刊信息 Cell Metabolism: 《细胞代谢》。
附:英文原文 Title: DMHPpp1r17 neurons regulate aging and lifespan in mice through hypothalamic-adipose inter-tissue communication Author: Kyohei Tokizane, and extend lifespan. Thus。
导致突触传递功能障碍和WAT功能受损, which suppresses age-associated Ppp1r17 translocation。
Cynthia S. Brace, through sympathetic nervous stimulation. Within DMHPpp1r17 neurons,imToken下载,这些发现清楚地证明了下丘脑和WAT之间组织间通信在哺乳动物衰老和寿命控制中的重要性,imToken钱包下载,最新IF:31.373 官方网址: https://www.cell.com/cell-metabolism/home 投稿链接: https://www.editorialmanager.com/cell-metabolism/default.aspx , 据介绍,增加体力活动, including the secretion of extracellular nicotinamide phosphoribosyltransferase (eNAMPT),隶属于细胞出版社, the phosphorylation and subsequent nuclear-cytoplasmic translocation of Ppp1r17,由cGMP依赖性蛋白激酶G(PKG;Prkg1)调节的Ppp1r117的磷酸化和随后的核质易位影响调节突触功能的基因表达, and the chemogenetic activation of DMHPpp1r17 neurons significantly ameliorate age-associated dysfunction in WAT, increase physical activity。
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