Suppr超能文献

晚期慢性心力衰竭患者心肌样本中的血管生成激活指数。

Indexes of Angiogenic Activation in Myocardial Samples of Patients with Advanced Chronic Heart Failure.

机构信息

Department of Medicine and Health Sciences, University of Molise, 86100 Campobasso, Italy.

Pulmonary Rehabilitation Unit and Laboratory of Cytoimmunopathology of the Heart and Lung, Istituti Clinici Scientifici Maugeri, 28010 Veruno, Italy.

出版信息

Medicina (Kaunas). 2019 Nov 29;55(12):766. doi: 10.3390/medicina55120766.

Abstract

: Ischemic and idiopathic heart failure are characterized by reactive cardiac fibrosis and impaired vasculogenesis involving pro-angiogenic factors such as angiogenin, angiopoietin-1 (Ang-1), and angiopoietin-2 (Ang-2), as demonstrated in experimental models of heart failure. However, differences in the molecular pathways between these cardiomyopathies are still unclear. In this short communication, we evaluate and compare the expression of pro-angiogenic molecules in the heart tissue of patients with advanced chronic heart failure (CHF) of ischemic vs. nonischemic etiology : We obtained heart tissue at transplantation from left ventricular walls of 16 explanted native hearts affected by either ischemic (ICM) or nonischemic dilated cardiomyopathy (NIDCM). Tissue samples were examined using immunohistochemistry for angiogenic molecules. : We found immunopositivity (I-pos) for angiopoietin-1 mainly in the cardiomyocytes, while we observed I-pos for Ang-2 and Tie-2 receptor mainly in endothelial cells. Expression of Procollagen-I (PICP), angiogenin, Ang-1, and Tie-2 receptor was similar in ICM and NIDCM. In contrast, endothelial immunopositivity for Ang-2 was higher in ICM samples than NIDCM ( = 0.03). : In our series of CHF heart samples, distribution of Ang-1 and angiogenin was higher in cardiomyocytes while that of Ang-2 was higher in endothelial cells; moreover, Ang-2 expression was higher in ICS than NIDCM. Despite the small series examined, these findings suggest different patterns of angiogenic stimulation in ICM and NIDCM, or at least a more altered endothelial integrity in ICD. Our data may contribute to a better understanding of the angiogenesis signaling pathways in CHF. Further studies should investigate differences in the biochemical processes leading to heart failure.

摘要

缺血性和特发性心力衰竭的特征是反应性心肌纤维化和血管生成受损,涉及促血管生成因子,如血管生成素、血管生成素-1(Ang-1)和血管生成素-2(Ang-2),这在心力衰竭的实验模型中得到了证实。然而,这些心肌病之间的分子途径的差异仍不清楚。在本短通讯中,我们评估和比较了缺血性和非缺血性病因导致的晚期慢性心力衰竭(CHF)患者心脏组织中促血管生成分子的表达:我们从 16 例接受左心室壁移植的移植心脏中获得了组织样本,这些心脏分别受到缺血性(ICM)或非缺血性扩张型心肌病(NIDCM)的影响。使用免疫组织化学方法检查血管生成分子的表达。我们发现,血管生成素-1的免疫阳性(I-pos)主要存在于心肌细胞中,而 Ang-2 和 Tie-2 受体的 I-pos 主要存在于内皮细胞中。原胶原蛋白-I(PICP)、血管生成素、Ang-1 和 Tie-2 受体的表达在 ICM 和 NIDCM 中相似。相比之下,ICM 样本中内皮细胞的 Ang-2 免疫阳性高于 NIDCM(=0.03)。在我们的 CHF 心脏样本系列中,Ang-1 和血管生成素在心肌细胞中的分布较高,而 Ang-2 在内皮细胞中的分布较高;此外,ICM 中的 Ang-2 表达高于 NIDCM。尽管检查的样本系列较小,但这些发现表明 ICM 和 NIDCM 中促血管生成刺激的模式不同,或者至少 ICM 中的内皮完整性更改变。我们的数据可能有助于更好地理解 CHF 中的血管生成信号通路。进一步的研究应调查导致心力衰竭的生化过程的差异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a9d/6956299/fa095f8bafbb/medicina-55-00766-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验