Hayashi Takeshi, Deguchi Kentaro, Nagotani Shoko, Zhang Hanzhe, Sehara Yoshihide, Tsuchiya Atsushi, Abe Koji
Department of Neurology, Okayama University Graduate School of Medicine and Dentistry, Japan.
Curr Neurovasc Res. 2006 May;3(2):119-29. doi: 10.2174/156720206776875902.
Angiogenesis occurs in a wide range of conditions. As ischemic tissue usually depends on collateral blood flow from newly produced vessels, acceleration of angiogenesis should be of therapeutic value to ischemic disorders. Indeed, therapeutic angiogenesis reduced tissue injury in myocardial or limb ischemia. In ischemic stroke, on the other hand, angiogenic factors often increase vascular permeability and thus may deteriorate tissue damage. In order to apply safely the therapeutic angiogenesis for ischemic stroke treatment, elucidating precise mechanism of brain angiogenesis is mandatory. In the present article, we review previous reports which investigated molecular mechanisms of angiogenesis. Endothelial cell mitogens, enzymes that degrade surrounding extracellular matrix, and molecules implicated in endothelial cells migration are induced rapidly in the ischemic brain. Their possible neuroprotective or injury exacerbating effects are discussed. Because therapeutic potential of angiogenic factors application had gained much attention, we here extensively reviewed relevant previous reports. In the future however, there is a need to consider angiogenesis in relation with regenerative medicine, as angiogenic factors sometimes possess neuron producing property.
血管生成发生在多种情况下。由于缺血组织通常依赖于新生成血管的侧支血流，血管生成的加速对缺血性疾病应具有治疗价值。事实上，治疗性血管生成可减少心肌或肢体缺血中的组织损伤。另一方面，在缺血性卒中中，血管生成因子常常增加血管通透性，因此可能会加重组织损伤。为了安全地将治疗性血管生成应用于缺血性卒中治疗，阐明脑内血管生成的确切机制是必不可少的。在本文中，我们回顾了以往研究血管生成分子机制的报告。内皮细胞有丝分裂原、降解周围细胞外基质的酶以及与内皮细胞迁移有关的分子在缺血脑中迅速被诱导。讨论了它们可能的神经保护或损伤加重作用。由于血管生成因子应用的治疗潜力备受关注，我们在此广泛回顾了以往的相关报告。然而，在未来，有必要将血管生成与再生医学联系起来考虑，因为血管生成因子有时具有产生神经元的特性。
