Arredondo-Damián Jeanette Guadalupe, Martínez-Soto Juan Manuel, Molina-Pelayo Francisco A, Soto-Guzmán Jesús Adriana, Castro-Sánchez Luis, López-Soto Luis Fernando, Candia-Plata Maria Del Carmen
Doctoral Program in Sciences (Chemical-Biological and Health), University of Sonora, Hermosillo, Sonora, Mexico.
Department of Medicine and Health Sciences, University of Sonora, Hermosillo, Sonora, Mexico.
Heliyon. 2024 Feb 5;10(3):e25537. doi: 10.1016/j.heliyon.2024.e25537. eCollection 2024 Feb 15.
Type 2 diabetes (T2D) is a complex metabolic ailment marked by a global high prevalence and significant attention in primary healthcare settings due to its elevated morbidity and mortality rates. The pathophysiological mechanisms underlying the onset and progression of this disease remain subjects of ongoing investigation. Recent evidence underscores the pivotal role of the intricate intercellular communication network, wherein cell-derived vesicles, commonly referred to as extracellular vesicles (EVs), emerge as dynamic regulators of diabetes-related complications. Given that the protein cargo carried by EVs is contingent upon the metabolic conditions of the originating cells, particular proteins may serve as informative indicators for the risk of activating or inhibiting signaling pathways crucial to the progression of T2D complications.
In this study, we conducted a systematic review to analyze the published evidence on the proteome of EVs from the plasma or serum of patients with T2D, both with and without complications (PROSPERO: CRD42023431464).
Nine eligible articles were systematically identified from the databases, and the proteins featured in these articles underwent Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. We identified changes in the level of 426 proteins, with CST6, CD55, HBA1, S100A8, and S100A9 reported to have high levels, while FGL1 exhibited low levels.
These proteins are implicated in pathophysiological mechanisms such as inflammation, complement, and platelet activation, suggesting their potential as risk markers for T2D development and progression. Further studies are required to explore this topic in greater detail.
2型糖尿病（T2D）是一种复杂的代谢性疾病，全球患病率高，因其发病率和死亡率上升而在初级卫生保健环境中受到广泛关注。该疾病发生和发展的病理生理机制仍是正在研究的课题。最近的证据强调了复杂的细胞间通讯网络的关键作用，其中细胞衍生的囊泡，通常称为细胞外囊泡（EVs），成为糖尿病相关并发症的动态调节因子。鉴于EVs携带的蛋白质货物取决于起源细胞的代谢条件，特定蛋白质可能作为激活或抑制对T2D并发症进展至关重要的信号通路风险的信息指标。
在本研究中，我们进行了一项系统综述，以分析已发表的关于T2D患者血浆或血清中EVs蛋白质组的证据，包括有并发症和无并发症的患者（PROSPERO：CRD42023431464）。
从数据库中系统地鉴定出9篇符合条件的文章，并对这些文章中描述的蛋白质进行了基因本体论（GO）和京都基因与基因组百科全书（KEGG）通路富集分析。我们确定了426种蛋白质水平的变化，据报道CST6、CD55、HBA1、S100A8和S100A9水平较高，而FGL1水平较低。
这些蛋白质与炎症、补体和血小板活化等病理生理机制有关，表明它们有可能作为T2D发生和发展的风险标志物。需要进一步研究以更详细地探讨这一主题。
