Sanders-Brown Center on Aging, Department of Anatomy and Neurobiology, University of Kentucky, 430 Sanders-Brown Building, 800 South Limestone Street, Lexington, KY 40536-0230, USA.
ACS Chem Neurosci. 2013 Mar 20;4(3):370-4. doi: 10.1021/cn300197y. Epub 2012 Dec 24.
The sad reality is that in the year 2012, people are still dying or suffering from the extreme morbidity of ischemic stroke. This tragedy is only compounded by the graveyard full of once promising new therapies. While it is indeed true that the overall mortality from stroke has declined in the United States, perhaps due to increased awareness of stroke symptoms by both the lay public and physicians, it is clear that better therapies are needed. In this regard, progress has been tremendously slowed by the simple fact that experimental models of stroke and the animals that they typically employ, rats and mice, do not adequately represent human stroke. Furthermore, the neuroprotective therapeutic approach, in which potential treatments are administered with the hope of preventing the spread of dying neurons that accompanies a stroke, typically fail for a number of reasons such as there is simply more brain matter to protect in a human than there is in a rodent! For this reason, there has been somewhat of a shift in stroke research away from neuroprotection and toward a neurorepair approach. This too may be problematic in that agents that might foster brain repair could be acutely deleterious or neurotoxic and vice versa, making the timing of treatment administration after stroke critical. Therefore, in our efforts to discover a new stroke therapy, we decided to focus on identifying brain repair elements that were (1) endogenously and actively generated in response to stroke in both human and experimental animal brains, (2) present acutely and chronically after ischemic stroke, suggesting that they could have a role in acute neuroprotection and chronic neurorepair, and (3) able to be administered peripherally and reach the site of stroke brain injury. In this review, I will discuss the evidence that suggests that perlecan domain V may be just that substance, a potential beacon of hope for stroke patients.
可悲的现实是,在 2012 年,人们仍然死于或遭受缺血性中风的极度病态。这种悲剧只是因为曾经充满希望的新疗法的墓地而更加复杂。虽然美国中风的总体死亡率确实有所下降,这也许是由于公众和医生对中风症状的认识有所提高,但显然需要更好的治疗方法。在这方面,实验性中风模型及其通常使用的动物(大鼠和小鼠)不能充分代表人类中风这一简单事实极大地减缓了进展。此外,神经保护治疗方法,其中潜在的治疗方法被给予,希望阻止伴随中风的死亡神经元的扩散,但由于在人类中需要保护的脑实质比啮齿动物中多,因此这种方法通常会因为多种原因而失败!出于这个原因,中风研究已经从神经保护转向神经修复方法。这也可能是有问题的,因为促进大脑修复的药物可能会对大脑造成急性损害或神经毒性,反之亦然,因此中风后治疗的时机非常关键。因此,在我们努力寻找新的中风治疗方法时,我们决定专注于识别那些(1)在人类和实验动物大脑中对中风有内源性和主动反应生成的、(2)在缺血性中风后急性和慢性存在的、表明它们可能在急性神经保护和慢性神经修复中发挥作用的、(3)能够通过外周给药并到达中风脑损伤部位的大脑修复元素。在这篇综述中,我将讨论表明肝素结合表皮生长因子样生长因子(HB-EGF)的外显子 7 可能是治疗中风的一种新方法的证据。