Jazwa Agnieszka, Florczyk Urszula, Grochot-Przeczek Anna, Krist Bart, Loboda Agnieszka, Jozkowicz Alicja, Dulak Jozef
Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.
Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.
Vascul Pharmacol. 2016 Nov;86:18-30. doi: 10.1016/j.vph.2016.09.003. Epub 2016 Sep 10.
Vascular endothelial growth factor (VEGF), as an endothelial cell-specific mitogen, is crucial for new blood vessels formation. Atherosclerosis affecting the cardiovascular system causes ischemia and functio laesa in tissues supplied by the occluded vessels. When such a situation occurs in the lower extremities, it causes critical limb ischemia (CLI) often requiring leg amputation. Low oxygen tension leads to upregulation of hypoxia-regulated genes (i.e. VEGF), that should help to restore the impaired blood flow. In CLI these rescue mechanisms are, however, often inefficient. Moreover, there are many contradictory reports showing either induction, no changes or even down-regulation of VEGF in specimens taken from patients with CLI, as well as in samples collected from animals subjected to hindlimb ischemia. Additionally, taking into account numerous experimental and clinical data demonstrating rather insufficient therapeutic potential of VEGF, we called into question the role of this protein in limb ischemia and vessel regeneration. In this review we are also summarizing several aspects which can influence VEGF expression and its measurement in the ischemic tissues.
血管内皮生长因子（VEGF）作为一种内皮细胞特异性有丝分裂原，对新血管形成至关重要。影响心血管系统的动脉粥样硬化会导致缺血以及闭塞血管所供应组织的功能损害。当这种情况发生在下肢时，会导致严重肢体缺血（CLI），常需进行截肢。低氧张力会导致缺氧调节基因（如VEGF）上调，这应有助于恢复受损的血流。然而，在CLI中，这些挽救机制往往效率低下。此外，有许多相互矛盾的报道显示，从CLI患者获取的标本以及从后肢缺血动物采集的样本中，VEGF要么被诱导，要么无变化，甚至下调。此外，考虑到众多实验和临床数据表明VEGF的治疗潜力相当不足，我们对这种蛋白质在肢体缺血和血管再生中的作用提出了质疑。在本综述中，我们还总结了几个可能影响VEGF在缺血组织中表达及其测量的方面。
