对外泌体在动脉粥样硬化中作用的新认识。

IF 4.5 2区 生物学 Q2 CELL BIOLOGY
Zena Wehbe, Maya Wehbe, Ali Al Khatib, Ali H Dakroub, Gianfranco Pintus, Firas Kobeissy, Ali H Eid
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引用次数: 0

摘要

动脉粥样硬化仍然是心血管疾病的主要诱因,也是全球发病率和死亡率的主要原因。尽管阐明了导致动脉粥样硬化病因发病机制的几个分子、生化和细胞方面的问题,但人们对这种疾病的发病和进展仍有许多不了解之处。新出现的证据支持外泌体在动脉粥样硬化的细胞基础中发挥作用。事实上,活化单核细胞的外泌体似乎加强了正反馈循环,促进了促炎症白细胞的招募。此外,外泌体除了能促进血管平滑肌细胞的增殖和侵袭外,还能诱导病变部位的血管新生和增加内皮的通透性,这是纤维斑块的两个重要特征。根据外泌体的来源和载体,外泌体还能诱导血凝块的形成,并导致动脉粥样硬化的其他特征。综上所述,人们越来越清楚地认识到,更好地了解外泌体的生物学特性对于阐明动脉粥样硬化的发病机制不可或缺,从而为这种疾病提供潜在的新治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Emerging understandings of the role of exosomes in atherosclerosis.

Atherosclerosis remains a major contributor to cardiovascular disease, the leading cause of global morbidity and mortality. Despite the elucidation of several molecular, biochemical, and cellular aspects that contribute to the etio-pathogenesis of atherosclerosis, much remains to be understood about the onset and progression of this disease. Emerging evidence supports a role for exosomes in the cellular basis of atherosclerosis. Indeed, exosomes of activated monocytes seem to accentuate a positive feedback loop that promotes recruitment of pro-inflammatory leukocytes. Moreover, in addition to their role in promoting proliferation and invasion of vascular smooth muscle cells, exosomes can also induce neovascularization within lesions and increase endothelial permeability, two important features of fibrous plaques. Depending on their sources and cargo, exosomes can also induce clot formation and contribute to other hallmarks of atherosclerosis. Taken together, it is becoming increasingly evident that a better understanding of exosome biology is integral to elucidating the pathogenesis of atherosclerosis, and may thus provide insight into a potentially new therapeutic target for this disease.

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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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