Angiogenin and SDF-1α serum concentration in patients with systemic sclerosis in relation to clinical status.

Angiogenin and SDF-1α serum concentration in patients with systemic sclerosis in relation to clinical status.
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DOI:
10.5114/aoms.2011.20610
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发表时间:
2011-02
期刊:
Archives of medical science : AMS
影响因子:
--
通讯作者:
Waszczykowska E
Waszczykowska E
中科院分区:
其他
文献类型:
--
作者:
Dziankowska-Bartkowiak B;Gerlicz-Kowalczuk Z;Waszczykowska E

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系统性硬化症(SSc)是一种结缔组织疾病,其特征是由于血管变化和皮肤和内脏器官过度纤维化引起的组织缺氧。在疾病过程中观察到对血管和内皮的损伤,以及血管稳态的失衡、血管生成和血管发生的损害。本研究的目的是研究SSc患者中促血管生成因子angiogenin和SDF-1α。从50例dSSc(弥漫性SSc)和lSSc(限制性SSc)患者和38例健康对照组患者中收集血清样本。我们探讨了:1)血清SDF-1α和血管生成素浓度在研究组中的差异; 2)SSc中趋化因子与疾病持续时间、雷诺现象、皮肤硬化和TSS(总皮肤评分)的相关性。SSc患者的血清血管生成素浓度在统计学上显著升高,疾病持续时间与雷诺现象、皮肤硬化或TSS之间无相关性。血清SDF-1α水平与各组间无显著性差异或无相关性。SSc患者血清中血管生成素浓度的增加可能证实了SSc过程中缺氧和血管灌注减少引起的内皮损伤,而不会促进代偿性血运重建。
Systemic sclerosis (SSc) is a connective tissue disorder characterized by tissue hypoxia due to vascular changes and excessive fibrosis of the skin and internal organs. Damage to blood vessels and endothelium, as well as imbalance of vascular homeostasis, impairment of angiogenesis and vasculogenesis are observed in the course of the disease. The aim of the study was to investigate the pro-angiogenic factors angiogenin and SDF-1α in patients with SSc. Serum samples were collected from 50 patients with dSSc (diffuse SSc) and lSSc (limited SSc) and from 38 patients used as a healthy control group. We explored: 1) how the serum concentrations of SDF-1α and angiogenin differ in the investigated groups; 2) the correlation among chemokines in SSc and the duration of the disease, Raynaud’s phenomenon, sclerosis of the skin and TSS (total skin score). Patients with SSc showed statistically significantly higher serum angiogenin concentration and there was no correlation between duration of the disease and Raynaud’s phenomenon, skin sclerosis or TSS. There was also no difference or no correlation between serum level of SDF-1α and the investigated groups. The increase in angiogenin concentration in the serum in patients with SSc may confirm endothelial damage caused by hypoxia and reduced vascular perfusion due to the course of SSc without contributing to compensatory revascularization.
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