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Neuronal apoptosis following cerebral ischaemia:pathophysiology and possible therapeutic implications

机译：脑缺血后神经元凋亡：病理生理学及可能​​的治疗意义

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Neuronal apoptosis following cerebral ischaemia has become an issue of extraordinary scientific interest in the past decade. Besides necrosis, this highly relevant pathomechanism has been shown to be markedly involved in the pathogenesis of delayed postischaemic neuronal damage. As a result, a variety of possible neuroprotective strategies and therapeutic options subsequent to cerebral ischaemia have emerged. This article provides an overview of the pathophysiologic mechanisms underlying delayed neuronal apoptotic degeneration after cerebral ischaemia. Based on these facts, selected therapeutic implications are discussed in detail.Recent findings from experimental studies have demonstrated a new therapeutic neuroprotective potential of pharmaceutical blockade of death-inducing ligands (e.g. Fas/CD95 ligand), enhancement of survival signal transduction with endogenous ligands (e.g. erythropoietin) and therapeutically modulating the balance between intracellular anti- and proapoptotic Bcl proteins with intriguing molecular techniques after cerebral ischaemia.Neuronal apoptosis is highly relevant in the pathophysiology of neurodegenerative disorders, neurotrauma and cerebral ischaemia/reperfusion. Within the past few years, a variety of therapeutic strategies have emerged based on our increasing knowledge of the pathophysiology of apoptosis. Whereas inhibition of single factors in apoptotic cascades (e.g. proteases) has produced rather unsatisfying results, new opportunities have emerged at the molecular level due to advances in molecular medicine. These approaches offer promising opportunities for neuroprotective therapeutic strategies subsequent to cerebral ischaemia. It is tempting to speculate that a combination ('cocktail') of these antiapoptotic interventions might even increase their neuroprotective potential.
机译：在过去的十年中，脑缺血后的神经元凋亡已成为非常重要的科学问题。除坏死外，这种高度相关的发病机制已显示出明显参与了缺血后神经元延迟性损害的发病机理。结果，出现了脑缺血后各种可能的神经保护策略和治疗选择。本文概述了脑缺血后延迟性神经元凋亡变性的病理生理机制。基于这些事实，详细讨论了选定的治疗意义。实验研究的最新发现表明，药物阻断死亡诱导配体（例如Fas / CD95配体），增强内源性配体的生存信号转导具有新的治疗神经保护潜力（脑缺血后，通过有趣的分子技术，调节细胞内抗凋亡蛋白Bcl和促凋亡蛋白Bcl之间的平衡。神经细胞凋亡与神经退行性疾病，神经创伤和脑缺血/再灌注的病理生理高度相关。在过去的几年中，基于我们对细胞凋亡的病理生理学的日益了解，出现了多种治疗策略。尽管对凋亡级联反应（例如蛋白酶）中的单个因子的抑制产生了相当不令人满意的结果，但是由于分子医学的进步，在分子水平上出现了新的机会。这些方法为脑缺血后的神经保护性治疗策略提供了有希望的机会。试图推测这些抗凋亡干预措施的组合（“鸡尾酒”）甚至可能增加其神经保护潜力。

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