摘要
这篇评论文章的目的是描述氧化应激如何影响心血管疾病发展。表观遗传机制与氧化应激,以及更可靠的氧化应激生物标志有关。这是多年来设计癌症治疗方案的重要潜在手段之一,旨在调节氧化应激增强 “体内”,从而减轻随之而来的动脉粥样硬化的负担。作为一个范例,我们描述一个肥胖的例子。在这个范例中,氧化应激之间的缠绕,由于热量过多,脂肪组织功能障碍引起的慢性轻度炎症和血小板激活使得动脉粥样硬化恶性循环。在心血管疾病(CVD)的病理学中,氧化应激是一个主要的发病机理。活性氧(ROS)-依赖的信号通路提示转录和表观遗传失调,诱发慢性低度炎症,血小板激活和内皮功能障碍。此外,提出了氧化生物标志物有潜在改善当前心血管疾病的防治机制。这些包括ROS-产生和/或抑制分子,ROS-修饰化合物,如F2-异前列素。也有越来越多的证据表明,非编码微RNA(mi-RNA)极度参与转录后细胞功能的调控,包括活性氧生成、炎症、调节细胞增殖,脂肪细胞的分化、血管生成和细胞凋亡。这些分子作为疾病的标志和干预的靶点有促进转化的可能性。最后,氧化应激是许多心血管的药品和保健品的研究靶点,主要包括抗糖尿病的药物,他汀类药物,对肾素-血管紧张素系统阻断剂、多酚等抗氧化剂。RO产生机制的进一步了解,他们的生物学作用以及潜在的治疗意义转化为有效心血管预防的措施。
关键词: 生物标记,炎症,肥胖,氧压,血小板激活。
Current Medicinal Chemistry
Title:Oxidative Stress Drivers and Modulators in Obesity and Cardiovascular Disease: From Biomarkers to Therapeutic Approach
Volume: 22 Issue: 5
Author(s): F. Santilli, M.T. Guagnano, N. Vazzana, S. La Barba and G. Davi
Affiliation:
关键词: 生物标记,炎症,肥胖,氧压,血小板激活。
摘要: This review article is intended to describe how oxidative stress regulates cardiovascular disease development and progression. Epigenetic mechanisms related to oxidative stress, as well as more reliable biomarkers of oxidative stress, are emerging over the last years as potentially useful tools to design therapeutic approaches aimed at modulating enhanced oxidative stress “in vivo”, thereby mitigating the consequent atherosclerotic burden. As a paradigm, we describe the case of obesity, in which the intertwining among oxidative stress, due to caloric overload, chronic low-grade inflammation induced by adipose tissue dysfunction, and platelet activation represents a vicious cycle favoring the progression of atherothrombosis. Oxidative stress is a major player in the pathobiology of cardiovascular disease (CVD). Reactive oxygen species (ROS)- dependent signaling pathways prompt transcriptional and epigenetic dysregulation, inducing chronic low-grade inflammation, platelet activation and endothelial dysfunction. In addition, several oxidative biomarkers have been proposed with the potential to improve current understanding of the mechanisms underlying CVD. These include ROS-generating and/or quenching molecules, and ROS-modified compounds, such as F2-isoprostanes. There is also increasing evidence that noncoding micro- RNA (mi-RNA) are critically involved in post- transcriptional regulation of cell functions, including ROS generation, inflammation, regulation of cell proliferation, adipocyte differentiation, angiogenesis and apoptosis. These molecules have promising translational potential as both markers of disease and site of targeted interventions. Finally, oxidative stress is a critical target of several cardioprotective drugs and nutraceuticals, including antidiabetic agents, statins, renin-angiotensin system blockers, polyphenols and other antioxidants. Further understanding of ROS-generating mechanisms, their biological role as well as potential therapeutic implications would translate into consistent benefits for effective CV prevention.
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F. Santilli, M.T. Guagnano, N. Vazzana, S. La Barba and G. Davi , Oxidative Stress Drivers and Modulators in Obesity and Cardiovascular Disease: From Biomarkers to Therapeutic Approach, Current Medicinal Chemistry 2015; 22 (5) . https://dx.doi.org/10.2174/0929867322666141128163739
DOI https://dx.doi.org/10.2174/0929867322666141128163739 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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