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An angiogenic switch in macrophages involving synergy between toll-like receptors 2, 4, 7, and 9 and adenosine A_2A receptors

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AMERICAN JOURNAL OF PATHOLOGY 2003年第2期163卷 711-721页

作者： Pinhal-Enfield, G Ramanathan, M Hasko, G Vogel, SN Salzman, AL Boons, GJ Leibovich, SJ Univ Med & Dent New Jersey New Jersey Med Sch Dept Cell Biol & Mol Med Newark NJ 07013 USA Univ Med & Dent New Jersey New Jersey Med Sch Dept Surg Newark NJ 07013 USA Univ Maryland Dept Microbiol & Immunol Baltimore MD 21201 USA Inotek Pharmaceut Corp Beverly MA USA Univ Georgia Complex Carbohydrate Res Ctr Athens GA 30602 USA

Adenosine A(2A) receptor (A(2A)R) agonists synergize with Escherichia coli (E. coli) LPS [toll-like receptor (TLR)4 agonist] to up-regulate vascular endothelial growth factor (VEGF) expression in murine macrophages. Here, we demonstrate that TLR2, TLR7. and TLR9, but not TLR3 and TLR5 agonists, also synergize with A(2A)AR agonists and adenosine to up-regulate VEGF, while simultaneously strongly down-regulating TNFalpha expression. in the absence of adenosine or A(2A)R agonists, Porphyromonas gingivalis (P. gingivalis) LPS and PAM(3)CAG (TLR2 agonists), resiquimod (R848) (TLR7 agonist), and non-methylated CpG DNA (TLR9 agonist) strongly up-regulate TNFalpha expression, with no effect on VEGF. In the presence of adenosine or A(2A)R agonists but not A(2A)R agonists, TLR2, 4, 7, and 9 agonists strongly up-regulate VEGF expression, while simultaneously down-regulating TNFalpha. C57BL/ 10ScN (TLR4 deletion mutant) macrophages produce TNFa in response to TLR2, 3, 7, and 9 agonists, but not the TLR4 agonist E. coli LPS. With adenosine or A(2A)R agonists, TLR2, 7, and 9, but not TLR4 agonists, also synergistically up-regulate VEGF, while down-regulating TNFalpha expression. Polyinosinic-polycytidilic acid (poly(I:C)) (TIR3 agonist) stimulates TNFalpha expression in macrophages from both C57BL/10ScSn and C57BL/10ScN mice, but has little effect on VEGF expression in the presence of adenosine or A(2A)R agonists. R-flagellins from Serratia marcescens (S. marcescens) and Salmonella muenchen (S. muenchen) do not stimulate TNFalpha expression in either C57BL/ 10ScSn or C57BL10/ScN mice, and have no effect on VEGF production in the presence of adenosine or A(2A)AR agonists. While adenosine and A(2A)AR agonists strongly down-regulate TNFalpha protein expression induced by TLR2, 3, 4, 7, and 9 agonists, TNFa mRNA and NF-kappaB activation are not reduced. We propose a novel signaling pathway in murine macrophages involving synergy between TLRs 2, 4, 7, and 9 and A(2A)Rs, that up-regula

关键词：腺嘌呤/类似物和衍生物腺嘌呤/药理学腺苷/药理学腺苷-5'-(N-乙基羧基酰胺)/药理学血管生成抑制剂/药理学细胞培养的 DNA结合蛋白质类/激动剂 DNA结合蛋白质类/代谢内皮生长因子/代谢酶抑制剂/药理学胞间信号肽类和蛋白质类/代谢脂多糖类/药理学脂蛋白类/代谢淋巴因子/代谢巨噬细胞腹膜/细胞学巨噬细胞腹膜/药物作用巨噬细胞腹膜/代谢膜糖蛋白类/激动剂膜糖蛋白类/遗传学膜糖蛋白类/代谢小鼠近交C57BL 小鼠基因敲除 NF-κB/代谢新生血管化生理性紫杉酚/药理学受体腺苷A2A 受体细胞表面/激动剂受体细胞表面/遗传学受体细胞表面/代谢受体嘌呤能P1/代谢 Toll样受体2 Toll样受体3 Toll样受体4 Toll样受体5 Toll样受体7 Toll样受体9 Toll样受体肿瘤坏死因子α/遗传学肿瘤坏死因子α/代谢增量调节/生理学血管内皮生长因子A 血管内皮生长因子类血管舒张药/药理学动物人类男(雄)性小鼠

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Survivin-dependent angiogenesis in ischemic brain - Molecular mechanisms of hypoxia-induced up-regulation

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AMERICAN JOURNAL OF PATHOLOGY 2003年第3期163卷 935-946页

作者： Conway, EM Zwerts, F Van Eygen, V DeVriese, A Nagai, N Luo, W Collen, D Flanders Interuniv Inst Biotechnol Ctr Transgene Technol & Gene Therapy Louvain Belgium Katholieke Univ Leuven Ctr Mol & Vasc Biol Louvain Belgium

Approaches to regulating angiogenesis in the brain, which may diminish parenchymal damage after stroke, are lacking. Survivin, the inhibitor of apoptosis protein, is up-regulated in vitro in vascular endothelial cells by angiogenic factors, including vascular endothelial cell growth factor (VEGF). To evaluate the in vivo role of survivin in the brain in response to hypoxia/ischemia, we used a mouse model of stroke and show that 2 days after permanent middle cerebral artery occlusion, survivin is uniquely expressed by microvessels that form in the peri-infarct and infarct regions. The extent of vascularization of the infarct is dependent on expression of survivin, since vessel density is significantly reduced in mice with heterozygous deficiency of the survivin gene (survivin +/- mice), even though infarct sizes were not different. Hypoxia alone induces survivin expression in the brain, by cultured endothelial cells and by embryonic stem cells, but this response is at least partially independent of VEGF, hypoxia inducible factor la, or placental growth factor. Delineating the spatiotemporal pattern of expression of survivin after stroke, and the molecular mechanisms by which this is regulated, may provide novel approaches to therapeutically optimize angiogenesis in a variety of ischemic disorders.

关键词：动脉闭塞性疾病/并发症动脉闭塞性疾病/代谢动脉闭塞性疾病/病理生理学血管/病理生理学脑/病理生理学脑缺血/并发症脑缺血/病因学脑缺血/病理生理学细胞培养的脑动脉内皮生长因子/代谢缺氧脑/病因学缺氧脑/代谢凋亡抑制蛋白质类胞间信号肽类和蛋白质类/代谢淋巴因子/代谢小鼠近交BALBC 小鼠转基因微管相关蛋白质类/代谢肿瘤蛋白质类新生血管化生理性氧/代谢增量调节血管内皮生长因子A 血管内皮生长因子类动物小鼠

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The renin-angiotensin system influences ocular endothelial cell proliferation in diabetes - Transgenic and interventional studies

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AMERICAN JOURNAL OF PATHOLOGY 2003年第1期162卷 151-160页

作者： Moravski, CJ Skinner, SL Stubbs, AJ Sarlos, S Kelly, DJ Cooper, ME Gilbert, RE Wilkinson-Berka, JL Univ Melbourne Dept Physiol Parkville Vic 3010 Australia St Vincents Hosp Dept Med Fitzroy Vic 3065 Australia Austin & Repatriat Med Ctr Dept Med Heidelberg West Australia

Neovascularization in the retina and iris of diabetic patients is a major cause of severe visual loss. However, study of these lesions is compromised by the lack of a comparable diabetic rodent model. Because the vasoactive and angiogenic agent, angiotensin H, is involved in diabetic microvascular disease, we aimed to determine whether endothelial cell proliferation could be induced in the retinae and irides of hypertensive transgenic (mRen-2)27 rats that display an enhanced extra-renal renin-angiotensin system (RAS), including the eye. Six-week-old Ren-2, spontaneously hypertensive, and Sprague-Dawley rats received either streptozotocin or control vehicle and were studied for 36 weeks. Additional nondiabetic and diabetic Ren-2 rats were treated throughout with the angiotensin-converting enzyme inhibitor lisinopril (LIS) (10 mg/kg/day in drinking water). Endothelial cell proliferation was only observed in retinae and irides of diabetic Ren-2 rats and was reduced with LIS. In diabetic Ren-2, vascular endothelial growth factor (VEGF) and VEGFR-2 mRNA were increased in retinae and irides and reduced with US. Diabetes activated ocular renin in Ren-2 but not Sprague-Dawley rats. The diabetic Ren-2 rat is a model of intraocular endothelial cell proliferation that can be attenuated by RAS blockade via VEGF-dependent pathways. RAS blockade is a potential treatment for vision-threatening diabetic microvascular complications.

关键词：血管紧张素转换酶抑制药/药理学动物基因修饰慢性病糖尿病实验性/化学诱导糖尿病实验性/并发症糖尿病实验性/病理学糖尿病视网膜病变/病因学糖尿病视网膜病变/病理学疾病模型动物内皮生长因子/遗传学内皮生长因子/代谢内皮血管/药物作用内皮血管/代谢内皮血管/病理学眼/代谢眼/病理学杂合子原位杂交胞间信号肽类和蛋白质类/遗传学胞间信号肽类和蛋白质类/代谢虹膜/血液供给虹膜/药物作用虹膜/病理学赖诺普利/药理学淋巴因子/遗传学淋巴因子/代谢 RNA 信使/代谢大鼠近交SHR 大鼠 Sprague-Dawley 肾素/遗传学肾素/代谢肾素-血管紧张素系统/药物作用肾素-血管紧张素系统/生理学视网膜/药物作用视网膜/病理学链脲菌素血管内皮生长因子A 血管内皮生长因子受体2/遗传学血管内皮生长因子受体2/代谢血管内皮生长因子类动物女(雌)性大鼠

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Generation of a syngeneic mouse model to study the effects of vascular endothelial growth factor in ovarian carcinoma

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AMERICAN JOURNAL OF PATHOLOGY 2002年第6期161卷 2295-2309页

作者： Zhang, L Yang, N Garcia, JRC Mohamed, A Benencia, F Rubin, SC Allman, D Coukos, G Univ Penn Ctr Res Reprod & Womens Hlth Philadelphia PA 19104 USA Univ Penn Mol & Cellular Biol Program Philadelphia PA 19104 USA Univ Penn Dept Genet Philadelphia PA 19104 USA Univ Penn Dept Obstet & Gynecol Div Gynecol Oncol Philadelphia PA 19104 USA Univ Penn Abramson Family Canc Res Inst Philadelphia PA 19104 USA

Vascular endothelial growth factor (VEGF) performs multifaceted functions in the tumor microenvironment promoting angiogenesis, suppressing anti-tumor immune response, and possibly exerting autocrine functions on tumor cells. However, appropriate syngeneic animal models for in vivo studies are lacking. Using retroviral transfection and fluorescence-activated cell sorting, we generated a C57BL6 murine ovarian carcinoma cell line that stably overexpresses the murine VEGF164 isoform and the enhanced green fluorescent protein. VEGF164 overexpression dramatically accelerated tumor growth and ascites formation, significantly enhanced tumor angiogenesis, and substantially promoted the survival of tumor cells in vivo. In vitro, VEGF164 overexpression significantly enhanced cell survival after growth factor withdrawal and conferred resistance to apoptosis induced by cisplatin through an autocrine mechanism. VEGF/green fluorescent protein-expressing tumors were not recognized by the adaptive immune system. After vaccination, a specific anti-tumor T-cell response was detected, but tumor growth was not inhibited. This engineered murine carcinoma model should prove useful in the investigation of the role of VEGF in modulating the tumor microenvironment and affecting the complex interactions among angiogenesis mechanisms, anti-tumor immune mechanisms, and tumor cell behavior at the natural state or during therapy in ovarian carcinoma.

关键词：抗肿瘤药/代谢细胞凋亡/生理学腹水/代谢癌症疫苗/免疫学癌症疫苗/代谢癌/免疫学癌/代谢癌/病理学细胞分离细胞移植顺铂/药理学疾病模型动物内皮生长因子/遗传学内皮生长因子/免疫学内皮生长因子/代谢流式细胞术绿色荧光蛋白质类免疫组织化学原位缺口末端标记胞间信号肽类和蛋白质类/遗传学胞间信号肽类和蛋白质类/免疫学胞间信号肽类和蛋白质类/代谢发光蛋白质类/遗传学发光蛋白质类/代谢淋巴因子/遗传学淋巴因子/免疫学淋巴因子/代谢小鼠近交C57BL 肿瘤转移肿瘤移植新生血管化病理性卵巢肿瘤/免疫学卵巢肿瘤/代谢卵巢肿瘤/病理学腹膜肿瘤/代谢腹膜肿瘤/病理学蛋白质亚型/遗传学蛋白质亚型/代谢重组融合蛋白质类/遗传学重组融合蛋白质类/代谢肿瘤细胞培养的血管内皮生长因子A 血管内皮生长因子类动物女(雌)性人类小鼠

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Angiotensin II induces connective tissue growth factor gene expression via calcineurin-dependent pathways

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AMERICAN JOURNAL OF PATHOLOGY 2003年第1期163卷 355-366页

作者： Finckenberg, P Inkinen, K Ahonen, J Merasto, S Louhelainen, M Vapaatalo, H Müller, D Ganten, D Luft, F Mervaala, E Univ Helsinki Inst Biomed FIN-00014 Helsinki Finland Univ Helsinki Hosp Res Lab FIN-00014 Helsinki Finland Humboldt Univ Fac Med Charite Franz Volhard Clin HELIOS Klinikum Berlin D-10098 Berlin Germany Max Delbruck Ctr Mol Med Berlin Germany

Connective tissue growth factor (CTGF) is a polypeptide implicated in the extracellular matrix synthesis. Previous studies have provided evidence that angiotensin II (Ang II) promotes collagen synthesis and regulates collage a degradation. We investigated whether or not CTGF mediates the profibrotic effects of Ang H in the heart and kidneys and the role of calcineurin-dependent pathways in CTGF gene regulation. In transgenic rats harboring human renin and angiotensinogen genes, Ang H induced an age-dependent increase in myocardial CTGF expression, which was 3.5-fold greater compared to normotensive Sprague Dawley (SD) rats. C-TGF overexpression correlated closely with the Ang H-induced rise in blood pressure. CTGF mRNA and protein were located predominantly in areas with leukocyte infiltration, myocardial, and vascular lesions and co-localized with TGFbeta(1), collagen I, and collagen III mRNA expressions. Ang II induced CTGF mRNA and protein to a lesser extent in the kidneys, predominantly in glomeruli, arterioles, and in the interstitium with ample inflammation. However, no expression was found in the right ventricle or pulmonary arteries. Blockade of calcineurin activity by cyclosporine A completely normalized Ang II-induced CTGF overexpression in heart and kidney, suppressed the inflammatory response, and mitigated Ang H-induced cell proliferation and apoptosis. in contrast, blockade of mTOR (target of rapamycin) pathway by everolimus, further increased the expression of CTGF even though everolimus ameliorated cell proliferation and T-cell-mediated inflammation. Our findings provide evidence that CTGF mediates Ang H-induced fibrosis in the heart and kidneys via blood pressure and calcineurin-dependent pathways.

关键词：血管紧张素Ⅱ/遗传学血管紧张素Ⅱ/代谢血压钙神经素/代谢胶原Ⅰ型/遗传学胶原Ⅰ型/代谢胶原Ⅲ型/遗传学胶原Ⅲ型/代谢环孢菌素/代谢基因表达调控心脏/解剖学和组织学即早蛋白质类/遗传学即早蛋白质类/代谢免疫抑制剂/代谢原位杂交胞间信号肽类和蛋白质类/遗传学胞间信号肽类和蛋白质类/代谢肾/解剖学和组织学肾/病理学生物基因修饰大鼠 Sprague-Dawley 肾素/遗传学肾素/代谢西罗莫司/类似物和衍生物西罗莫司/代谢转化生长因子β/遗传学转化生长因子β/代谢转化生长因子β1 动物人类男(雄)性大鼠

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结缔组织生长因子在胃癌组织中的表达及其与预后的关系

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中国误诊学杂志 2008年第10期8卷 2274-2276页

作者：刘鲁英吴淑华赵铭锋吕增华朱玉红滨州医学院病理学教研室山东滨州256603 滨州医学院附属医院病理科山东滨州256603

目的:检测结缔组织生长因子(CTGF)在胃癌组织中的表达并探讨CTGF表达在患者预后判断中的意义。方法:应用免疫组织化学染色方法检测108例胃癌组织中CTGF的表达情况,分析CTGF表达与患者临床病理特征、术后生存时间之间的关系。结果:CTGF... 详细信息

目的:检测结缔组织生长因子(CTGF)在胃癌组织中的表达并探讨CTGF表达在患者预后判断中的意义。方法:应用免疫组织化学染色方法检测108例胃癌组织中CTGF的表达情况,分析CTGF表达与患者临床病理特征、术后生存时间之间的关系。结果:CTGF高表达常见于发生淋巴结转移的病例(P=0.038),CTGF表达水平低的患者术后五年生存率(48.4%)显著高于表达水平高的患者(23.9%,双侧log-rank检验,P=0.003 5)。Cox回归分析证明患者TNM分期(P<0.001)、肿瘤分化(P=0.027)和CTGF表达水平(P=0.016)是胃癌的独立预后因子。结论:胃癌组织中CTGF高表达与发生淋巴结转移和患者预后不良显著相关。

关键词：即早蛋白质类/代谢胞间信号肽类和蛋白质类/代谢胃肿瘤/代谢/诊断淋巴转移预后人类

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TSGF在原发性肝癌TACE治疗中疗效评估的应用价值

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中国医师杂志 2017年第2期19卷 253-256页

作者：李秀荣内蒙古医科大学附属医院保健科呼和浩特市010050

目的研究肿瘤特异性生长因子（TSGF）在原发性肝癌经肝动脉灌注化疗栓塞术（TACE）治疗前后的水平变化及其在疗效评估中的应用价值。方法选择2012年1月至2014年12月在内蒙古医科大学附属医院原发性肝癌患者75例，所有患者行TACE。监测... 详细信息

目的研究肿瘤特异性生长因子（TSGF）在原发性肝癌经肝动脉灌注化疗栓塞术（TACE）治疗前后的水平变化及其在疗效评估中的应用价值。方法选择2012年1月至2014年12月在内蒙古医科大学附属医院原发性肝癌患者75例，所有患者行TACE。监测术前、术后1周、术后1个月和术后3个月肝功能、血常规、甲胎蛋白（AFP）、TSGF水平变化，并进行疗效评定。结果（1）术后1周ALT、AST水平明显高于术前，而术后1个月与术前比较差异元统计学意义（P〉0．05）；术前术后WBC水平差异无统计学意义（P〉0．05）。（2）术后1周AFP、TSGF水平比术前明显升高（均P〈0．05），而术后1个月显著下降。（3）术后1个月CR＋PR＋SD与PD患者的AFP、TSGF水平比较差异无统计学意义（P〉0．05），术后3个月CR＋PR＋SD患者的AFP、TSGF水平显著低于PD患者（P〈0．05）。（4）CR＋PR＋SD患者术后3个月AFP、TSGF水平低于术前，而PD组患者治疗后不同时间AFP、TSGF水平差异无统计学意义（P〉0．05）。（5）术前不同AFP水平组在TACE治疗前后1个月AFP水平比较差异均无统计学意义（P〉0．05），而TACE治疗后1个月TSGF水平均显著低于治疗前，差异均有统计学意义（均P〈0．05）。结论TSGF水平在原发性肝癌患者进行TACE治疗过程中先上升后下降，尤其是治疗后1个月水平与肿瘤恶化情况有关。TSGF检测联合AFP、常规CT检查对原发性肝癌TACE治疗的远期疗效的评估有较高的应用价值。

关键词：胞间信号肽类和蛋白质类/代谢生长物质/代谢肝肿瘤/治疗化学栓塞治疗性肝动脉

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先天性肾积水组织的超微结构及CTGF表达定位的电镜观察

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中国医师杂志 2016年第9期18卷 1393-1395页

作者：窘产信刘永东李俊峰张传光张广平商希峰胡强潍坊市人民医院血管外科山东省潍坊261041 潍坊市人民医院小儿外科山东省潍坊261041 潍坊医学院山东省潍坊261053

目的研究肾盂输尿管连接部梗阻（UPJO）引起的先天性肾积水组织的超微结构变化及结缔组织生长因子（CTGF）在先天性肾积水中的表达定位。方法分别留取肾积水患儿5例、对照组2例组织标本，先用透射电镜观察超微结构的变化，再用胶体金做... 详细信息

目的研究肾盂输尿管连接部梗阻（UPJO）引起的先天性肾积水组织的超微结构变化及结缔组织生长因子（CTGF）在先天性肾积水中的表达定位。方法分别留取肾积水患儿5例、对照组2例组织标本，先用透射电镜观察超微结构的变化，再用胶体金做示踪物对病变组织进行免疫电镜观察，观察标记物所在位置，了解其在不同组织表达的差异性。结果透射电镜：积水肾实质细胞核间隙局部增宽，滤过膜的基质局部变薄、裂孔膜部分缺如、细胞核核型、核仁不规则，有较多自噬体。免疫电镜：CTGF在患肾的肾实质、肾盂、肾盂输尿管连接处狭窄段中的表达均明显增高，成纤维细胞细胞超微结构清晰，金颗粒呈团状、点灶状分布，特异性强，CTGF蛋白阳性标记主要位于粗面内质网、细胞核、核膜、线粒体等部位。结论先天性肾积水的形成与组织纤维化密切相关，CTGF与先天性肾积水的形成之间有相关性，在其发病过程中可能发挥重要作用。

关键词：肾盂积水/先天性/代谢/病理学胞间信号肽类和蛋白质类/代谢显微镜检查电子

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脂肪细胞因子在非酒精性脂肪性肝病中的作用

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中国误诊学杂志 2010年第12期10卷 2784-2785页

作者：杨淼李异玲中国医科大学附属第一医院消化内科辽宁沈阳110001

目的:探讨脂肪细胞因子瘦素、脂联素在非酒精性脂肪性肝病发病及其发展中的作用。方法:NAFLD患者60例与健康组60例相对照,ELISA法测定血清瘦素、脂联素水平。结果:NAFLD组与对照组相比,血清瘦素水平明显高于对照组(P<0.01),脂联素水... 详细信息

目的:探讨脂肪细胞因子瘦素、脂联素在非酒精性脂肪性肝病发病及其发展中的作用。方法:NAFLD患者60例与健康组60例相对照,ELISA法测定血清瘦素、脂联素水平。结果:NAFLD组与对照组相比,血清瘦素水平明显高于对照组(P<0.01),脂联素水平明显低于对照组(P<0.01)。结论:NAFLD患者血清瘦素水平升高,血清脂联素水平降低,这两种细胞因子均与胰岛素抵抗相关。

关键词：脂细胞脂肪肝/代谢瘦素/代谢胞间信号肽类和蛋白质类/代谢

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慢性心力衰竭急性加重患者血清生长分化因子-15水平及其对预后的评估意义

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中国医师杂志 2016年第5期18卷 680-683,687页

作者：关敬树周云缪志静张超施珊岚上海宝山中西医结合医院心内科上海201900

目的探讨慢性心力衰竭（CHF）急性加重患者血清生长分化因子-15（GDF-15）水平及其与常用指标的相关性,旨在为CHF的临床诊疗和预后判断提供参考.方法选取CHF急性加重患者200例,设为CHF组;另匹配性选取健康志愿者100例,设为对照组.CH... 详细信息

目的探讨慢性心力衰竭（CHF）急性加重患者血清生长分化因子-15（GDF-15）水平及其与常用指标的相关性,旨在为CHF的临床诊疗和预后判断提供参考.方法选取CHF急性加重患者200例,设为CHF组;另匹配性选取健康志愿者100例,设为对照组.CHF组患者分别于入院2h内、症状好转出院前,对照组受试者于体检当日,检测血清GDF-15、N末端脑钠肽原（NT-proBNP）水平,进行超声心动图检查以测量左室收缩末期内径（LVESD）、左室舒张末期内径（LVEDD）,计算左室射血分数（LVEF）.随访2年记录CHF相关不良事件.Spearman相关分析检验GDF-15与其他指标间的相关性,绘制受试者工作特征曲线（ROC）并计算曲线下面积（AUC）以分析评估指标诊断CHF的价值.结果 CHF组患者各时点血清GDF-15及NT-proBNP水平均高于对照组（t =4.70-7.11,P＜0.05或P＜0.01）,血清GDF-15、NT-proBNP水平与LVEF均呈负相关（r=-0.539、-0.572,P＜0.01）,与LVESD、LVEDD、NYHA心功能分级均呈正相关（r=0.505 -0.861,P＜0.01）;血清GDF-15与NT-proBNP水平呈正相关（r=0.528,P＜0.01）.随着血清GDF-15水平升高,再入院率、死亡率增高（χ^2=36.86、26.59,P＜0.01）.血清GDF-15预测再入院风险的AUC为0.822（95％ CI：0.719 -0.890,P＜0.01）,最佳预测截点为2876.30ng/L（敏感度为91.86％,特异度为73.27％）;预测死亡风险的AUC为0.816（95％ CI：0.715 -0.885,P＜0.01）,最佳预测截点为3487.05ng/L（敏感度为91.72％,特异度为69.05％）.结论 CHF急性加重患者血清GDF-15水平较高,随着症状好转而降低,且与NT-proBNP、NYHA心功能分级均呈正相关,与LVEF呈负相关,在预测CHF相关不良事件风险方面具有较高的敏感度,其机制可能与激活SMAD通路有关,在心血管系统疾病的临床诊疗和预后判断方面可能是比较有前景的生物标记物.

关键词：心力衰竭/代谢胞间信号肽类和蛋白质类/代谢预后

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