Molecular/Cancer Biology Program and Finnish Institute for Molecular Medicine, University of Helsinki, Helsinki, Finland.
J Clin Invest. 2011 Jun;121(6):2157-9. doi: 10.1172/JCI58196. Epub 2011 May 23.
Twenty years after the discovery of the vascular endothelial Tie receptor tyrosine kinases and 15 years after the discovery of the Tie2 ligand, angiopoietin-1 (Angpt1, also known as Ang1), a study published in the current issue of the JCI reveals an unexpected loss-of-function phenotype of mice conditionally deleted of the Angpt1 gene. The results suggest that Angpt1 is needed as a vascular stabilizing factor that organizes and limits the angiogenesis response and protects from pathological consequences, such as tissue fibrosis.
在发现血管内皮 Tie 受体酪氨酸激酶 20 年后，以及发现 Tie2 配体 15 年后，一项发表在本期《临床研究杂志》上的研究揭示了条件性敲除 Angpt1 基因的小鼠出现了一种意想不到的功能丧失表型。研究结果表明，Angpt1 作为一种血管稳定因子是必需的，它可以组织和限制血管生成反应，并防止组织纤维化等病理性后果。
