White Melanie Y, Van Eyk Jennifer E
Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21224, USA.
Mol Diagn Ther. 2007;11(2):83-95. doi: 10.1007/BF03256227.
With cardiovascular (CV)-related disorders accounting for the highest mortality rates in the world, affecting the quantity and quality of life of patients and creating an economic burden of prolonged therapeutic intervention, there is great significance in understanding the cellular and molecular alterations that influence the progression of these pathologies. The cellular genotype is regulated by the DNA component, whilst the cellular phenotype is influenced by the protein complement. By improving the understanding of the molecular mechanisms that influence the protein profile, the pathologies that influence the intrinsic functions of the CV system may be detected earlier or managed more efficiently. This is achievable with technologies encompassed by 'proteomics.' Proteomic investigations of CV diseases, including dilated cardiomyopathy (DCM), atherosclerosis, and ischemia/reperfusion (I/R) injury, have identified candidate proteins altered with the pathologic states, complementing past biochemical and physiologic observations. Whilst proteomics is still a relatively new discipline to be applied to the basic scientific investigation of CV diseases, it is emerging as a technique to screen for potential biomarkers in both tissues/cells and biologic fluids (biofluids), as well as to identify the targets of existing therapeutics. By enabling the separation of complex mixtures over numerous dimensions, exploiting the intrinsic properties of proteins, including charge state, molecular mass, and hydrophobicity, in addition to cellular location, the discrete alterations within the cell may be resolved. Proteomics has shown alterations to myofilament proteins including troponin I and myosin light chain, correlating with the reduction in contractility in the myocardium from DCM and I/R. The diverse cell types that coalesce to induce atherosclerotic plaque formation have been investigated both collectively and individually to elucidate the influence of the modifications to single cell types on the developing plaque as a whole. Proteomics has also been used to observe changes to biofluids occurring with these pathologies, a new potential link between basic science and clinical applications. The development of CV proteomics has helped to identify a number of possible protein candidates, and offers the potential to treat and diagnose CV disease more effectively in the future.
心血管(CV)相关疾病在全球死亡率中占比最高,影响患者的生活质量和数量,并造成长期治疗干预的经济负担。因此,了解影响这些疾病进展的细胞和分子变化具有重要意义。细胞基因型由DNA成分调节,而细胞表型受蛋白质组成的影响。通过增进对影响蛋白质谱的分子机制的理解,可以更早地检测出影响CV系统内在功能的疾病,或更有效地进行管理。这可以通过“蛋白质组学”所涵盖的技术来实现。对包括扩张型心肌病(DCM)、动脉粥样硬化和缺血/再灌注(I/R)损伤在内的CV疾病的蛋白质组学研究,已经确定了随病理状态改变的候选蛋白质,补充了过去的生化和生理学观察结果。虽然蛋白质组学在应用于CV疾病的基础科学研究方面仍是一个相对较新的学科,但它正逐渐成为一种在组织/细胞和生物体液(生物流体)中筛选潜在生物标志物以及识别现有治疗靶点的技术。通过在多个维度上分离复杂混合物,利用蛋白质的内在特性,包括电荷状态、分子量和疏水性,以及细胞定位,可以解析细胞内的离散变化。蛋白质组学已显示肌丝蛋白(包括肌钙蛋白I和肌球蛋白轻链)发生改变,这与DCM和I/R导致的心肌收缩力降低相关。为了阐明对单个细胞类型的修饰对整个发展中的斑块的影响,已经对聚集形成动脉粥样硬化斑块的多种不同细胞类型进行了集体和单独研究。蛋白质组学还被用于观察这些疾病在生物体液中发生的变化,这是基础科学与临床应用之间的一个新的潜在联系。CV蛋白质组学的发展有助于识别许多可能的蛋白质候选物,并为未来更有效地治疗和诊断CV疾病提供了潜力。