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1.
赵莎莎  高超  陶凌 《心脏杂志》2016,28(3):341-343
CTRP3是C1q肿瘤坏死因子相关蛋白家族中的一员,是新发现的脂肪因子。研究发现CTRP3在抗炎、代谢调控及减轻缺血损伤等方面发挥重要作用。本文就CTRP3的分子结构、表达、含量以及生物功能做一综述。  相似文献   

2.
C1q/肿瘤坏死因子相关蛋白9(CTRP9)是蛋白超家族-C1q/肿瘤坏死因子相关蛋白家族的核心成员之一,主要表达于脂肪组织。近年来,许多研究表明,CTRP9的异常表达与T2DM、肥胖、MS、动脉粥样硬化等疾病关系密切。本文对CTRP9分泌和作用通路及其与代谢相关疾病的研究进展进行综述。  相似文献   

3.
补体1q肿瘤坏死因子相关蛋白(CTRP)9是CTRP蛋白家族重要成员,与脂联素高度同源,结构相似。近几年发现CTRP9在动脉粥样硬化、缺血性心脏病(IHD)等心血管疾病中作用广泛。除了经典的调节糖脂代谢、调节内皮功能外,最近的研究显示外源性补充CTRP9能够对缺血心肌发挥保护作用,而且CTRP9在心脏局部特异性高表达,可能是一种重要的心脏因子,参与调节心肌局部微环境,发挥心肌保护作用,本文将就CTRP9在心血管保护方面的研究进展进行综述。  相似文献   

4.
感染性和炎症性疾病常伴有代谢改变,代谢相关脂肪性肝病(MAFLD)和T2DM特点是具有高水平的促炎细胞因子.补体C1q/TNF相关蛋白(CTRPs)的APN家族因抗炎和Ins增敏作用引起关注.CTRP3、CTRP5、CTRP9、CTRP13可通过调节代谢途径、影响免疫炎症反应控制MAFLD和T2DM的发生发展.本文对C...  相似文献   

5.
C1q肿瘤坏死因子相关蛋白(C1q/tumor necrosis factor-related proteins,CTRPs)是一类新发现的蛋白超家族,与脂联素具有高度同源性。CTRPs组织分布广泛,生物学功能多样,参与调节物质代谢、血管壁细胞功能、血小板聚集、炎性反应等。CTRP4是该家族成员之一,其结构特殊,包含2个球状C1q结构域,缺乏胶原结构域。CTRP4对肿瘤、代谢、炎症及心血管疾病有重要调节作用。该文介绍CTRP4的结构特点、分布表达及其生物学功能。  相似文献   

6.
C1q/肿瘤坏死因子相关蛋白9(C1q/TNF-related protein 9,CTRP9)是一种新发现的与脂联素高度同源的脂肪细胞因子,其对机体具有正性作用,在调节代谢、保护心肌、舒张血管和改善内皮功能等方面发挥重要作用。本文对CTRP9的分子结构、聚合形式、组织表达和分泌以及生物学功能作一综述。  相似文献   

7.
C1q-肿瘤坏死因子相关蛋白3(CTRP3)是C1q肿瘤坏死因子相关蛋白家族中的一员。研究发现,CTRP3不仅具有抗炎、减轻缺血损伤的作用,而且可以对抗IR,增加IS。本文就CTRP3与IR相关性疾病间的研究进展做一综述。  相似文献   

8.
C1q肿瘤坏死因子相关蛋白3是新近发现的C1q肿瘤坏死因子相关蛋白家族中的一员。近年来发现它在糖脂代谢、动脉粥样硬化、肥胖、高血压、促进缺血心肌新生血管形成等心血管疾病方面发挥作用。文章将对C1q肿瘤坏死因子相关蛋白3在心血管疾病方面的研究进展做一综述。  相似文献   

9.
C1q/肿瘤坏死因子相关蛋白9(C1q/TNF-related protein9,CTRP9)是一种新发现的与脂联素高度同源的脂肪细胞因子,其对机体具有正性作用,在调节代谢、保护心肌、舒张血管和改善内皮功能等方面发挥重要作用。本文对CTRP9的分子结构、聚合形式、组织表达和分泌以及生物学功能作一综述。  相似文献   

10.
<正>C1q肿瘤坏死因子相关蛋白(C1q/Tumor necrosis factor related proteins, CTRP)是脂肪组织分泌的、与同为其分泌的脂联素有高度同源性的蛋白。单个CTRP存在4个独立结构域:短的可变区、N-末端信号肽、C-末端球形区域、胶原样区域。作为与脂联素结构最为相似的CTRP蛋白家族成员CTRP9,参与血糖调控、能量代谢、血管舒张、改善内皮功能等多方面的调节作用。CTRP9对于心、  相似文献   

11.
刘敏  彭铤  肖新华 《中国动脉硬化杂志》2019,27(3):264-266, 272
C1q/肿瘤坏死因子相关蛋白6(CTRP6)是CTRP超家族中的一员,诸多研究证明,CTRP在胰岛素抵抗及肥胖的形成中起到重要作用,因而研究其参与的作用及具体机制,有助于为胰岛素抵抗及肥胖的治疗指明方向。文章主要对CTRP6的结构、分布及其促进胰岛素抵抗与肥胖的相关生理功能的研究进展进行综述。  相似文献   

12.
C1q/TNF-related protein-3 (CTRP3) is a novel adipokine with anti-inflammatory and a multitude of biological effects on glucose and lipid metabolism however, the influence of CTRP3 on incidence of diabetes mellitus remain unclear. This study investigated the effects of CTRP3 levels in obese and normal body weight young adults on insulin resistance and occurrence of diabetes mellitus.Subjects and methodsIn this case control study, Serum levels of CTRP3, HbA1c, Lipid profile, glucose and insulin levels were determined in 75 obese and 68 normal body weight individuals.ResultsIn obese young adults CTRP3 concentrations were decreased compared to normal body weight young adults (NBW). The association between reduction of CTRP3 concentrations and the presence of diabetes is statistically significant. CTRP3 showed significant negative correlation with BMI, HOMA-IR and triglycerides as well as positive correlations with HDL – cholesterol while there is no association between CTRP3 and BMI within the NBW group. Higher HbA1C, HOMA-IR, and risk of diabetes development within obese subjects were related to lower CTRP3 concentration.ConclusionsThis study shows that reduction of CTRP3 concentrations is likely to bring a concomitant increase in risk of diabetes in obese and normal body weight young adults. Decrease in CTRP3 concentration may have an essential role in the pathophysiology of metabolic disorders concomitant to obesity.  相似文献   

13.
Adipokines are cytokines produced by adipocytes that may mediate inflammatory processes, whilst adipocyte-derived proteins may have the converse effect. C1q/TNF-related protein-3 or CTRP3 is a novel adipokine that is expressed and released by most types of human tissues including adipose tissue. This adipokine, considered as an adiponectin, can normalize blood glucose by several mechanisms. In addition, it can modulate the expression/secretion of other cytokine and adipokines leading to lower insulin resistance in peripheral tissues. Beneficial effects of CTRP3 against hyperglycemia-induced complications in the kidney and eye have been reported. In this review, we have presented the latest findings on the in vitro and in vivo hypoglycemic effects of CTRP3, followed by the findings on the preventive/therapeutic effects of CTRP3 adipokines against diabetes related complications.  相似文献   

14.
C1q/肿瘤坏死因子相关蛋白(CTRP) 12是一种新型脂肪因子,属于CTRP超家族成员.其主要在脂肪组织表达及分泌,通过增强脂肪组织和肝脏中胰岛素信号,改善胰岛素抵抗,增加胰岛素敏感性.同时CTRP12还能降低脂肪组织炎性反应.CTRP12通过胰岛素依赖和非依赖的方式发挥作用,有望成为治疗胰岛素抵抗和2型糖尿病的新靶点.  相似文献   

15.
心肌梗死后的心肌重构是一个复杂的病理过程,严重影响患者预后。CTRP9是近年来新发现的脂肪因子,大量研究表明CTRP9可抑制心肌梗死后心肌重构,本文就CTRP9对心肌梗死后心肌重构的相关研究作一综述。  相似文献   

16.
目的:探讨血清补体C1q肿瘤坏死因子相关蛋白9(CTRP9)表达水平与冠心病的关系。方法:入选经冠状动脉造影证实的稳定型冠心病患者278例(冠心病组)和113例健康对照(对照组),采用酶联免疫吸附法(ELISA)检测血清中CTRP9的水平。结果:冠心病组CTRP9水平明显低于对照组(P〈0.05);多元逻辑回归分析发现,CTRP9降低是冠心病的独立危险因素。结论:血清CTRP9水平降低与冠心病发生有关,CTRP1降低是冠心病的独立危险因素。  相似文献   

17.
目的探讨阻塞性睡眠呼吸暂停(OSA)合并原发性醛固酮增多症(PA)患者血清补体C1q肿瘤坏死因子相关蛋白1(CTRP1)的水平及其相关因素。方法病例组选取高血压住院患者中诊断为OSA合并PA患者28例,对照组选取同期入院的诊断为高血压合并OSA的患者30例,放射免疫法测定血浆肾素活性(PRA)、血管紧张素Ⅱ(AngⅡ)及血清醛固酮水平、酶联免疫吸附法检测CTRP1浓度。结果 OSA合并PA组的醛固酮水平与OSA组相比差异有统计学意义(P<0.05),CTRP1、PRA、AngⅡ、C反应蛋白(CRP)、血钾及血钠在2组间差异无统计学意义。Pearson相关分析显示,在总体人群中CTRP1与睡眠呼吸紊乱指数(AHI)、醛固酮及其他OSA及PA的相关因素均不相关,但在OSA合并PA人群中,CTRP1与AngⅡ呈负相关(r=-0.458,P<0.05)。结论高血压患者中,OSA并PA血清CTRP1水平与OSA人群相比差异无统计学意义。在OSA合并PA人群中,CTRP1水平与AngⅡ呈负相关,与醛固酮水平无关。  相似文献   

18.
Maintaining proper energy balance in mammals entails intimate crosstalk between various tissues and organs. These inter-organ communications are mediated, to a great extent, by secreted hormones that circulate in blood. Regulation of the complex metabolic networks by secreted hormones (e.g., insulin, glucagon, leptin, adiponectin, FGF21) constitutes an important mechanism governing the integrated control of whole-body metabolism. Disruption of hormone-mediated metabolic circuits frequently results in dysregulated energy metabolism and pathology. As part of an effort to identify novel metabolic hormones, we recently characterized a highly conserved family of 15 secreted proteins, the C1q/TNF-related proteins (CTRP1-15). While related to adiponectin in sequence and structural organization, each CTRP has its own unique tissue expression profile and non-redundant function in regulating sugar and/or fat metabolism. Here, we summarize the current understanding of the physiological functions of CTRPs, emphasizing their metabolic roles. Future studies using gain-of-function and loss-of-function mouse models will provide greater mechanistic insights into the critical role CTRPs play in regulating systemic energy homeostasis.  相似文献   

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