Kaneez Fatima Shad, Nazar Luqman, Ann M Simpson, Sara Lal
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引用次数: 3
摘要
动脉粥样硬化是大多数心肌梗死(MI)和缺血性脑卒中发作的潜在原因。动脉粥样硬化的早期征兆是动脉壁肥大。众所周知,内膜中膜厚度(IMT)的增加是动脉壁改变的非侵入性标志,可以通过高分辨率b超在颈动脉中轻松评估。同样,心肌梗死和缺血性中风的另一个关键因素是n -甲基- d -天冬氨酸(NMDA)受体,它是一种嗜离子性谷氨酸受体,介导大脑中绝大多数兴奋性神经传递。NMDA的激活需要谷氨酸和像d -丝氨酸这样的凝聚剂结合到它的甘氨酸位点上。l -丝氨酸转化为d -丝氨酸需要一种特殊的酶,丝氨酸消旋酶(SR), SR活性的改变会导致各种生理和病理状况,从突触可塑性到缺血、心肌梗死和中风。可用于激活谷氨酸信号的d -丝氨酸的数量在很大程度上取决于SR,我们已经开发出了估算其在人类血液样本中的水平并将其与IMT相关联的方法。这项基于短通信的研究描述了我们的初步研究,它清楚地表明SR、d -丝氨酸和IMT之间存在直接关系。在这篇文章中,我们将讨论SR的活性是否可以决定心肌梗死和中风等血管病变的未来后果。
Atherosclerosis is the underlying cause of most myocardial infarction (MI) and ischaemic stroke episodes. An early sign of atherosclerosis is hypertrophy of the arterial wall. It is known that increased intima media thickness (IMT) is a non-invasive marker of arterial wall alteration, which can easily be assessed in the carotid arteries by high-resolution B-mode ultrasound. Similarly, the other key element of MI and ischaemic strokes is the N-methyl-D-aspartate (NMDA) receptor which is an ionotropic glutamate receptor that mediates the vast majority of excitatory neurotransmission in the brain. NMDA activation requires the binding of both glutamate and a coagonist like D-serine to its glycine site. A special enzyme, serine racemase (SR), is required for the conversion of L-serine into D-serine, and alterations in SR activities lead to a variety of physiological and pathological conditions ranging from synaptic plasticity to ischemia, MI, and stroke. The amount of D-serine available for the activation of glutamatergic signalling is largely determined by SR and we have developed ways to estimate its levels in human blood samples and correlate it with the IMT. This research based short communication describes our pilot study, which clearly suggests that there is a direct relationship between the SR, D-serine, and IMT. In this article, we will discuss whether the activity of SR can determine the future consequences resulting from vascular pathologies such as MI and stroke.