Angelini Francesco, Pagano Francesca, Bordin Antonella, Milan Marika, Chimenti Isotta, Peruzzi Mariangela, Valenti Valentina, Marullo Antonino, Schirone Leonardo, Palmerio Silvia, Sciarretta Sebastiano, Murdoch Colin E, Frati Giacomo, De Falco Elena
Department of Medical Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy.
Institute of Cell Biology and Neurobiology-CNR, Monterotondo, Rome, Italy.
Oxid Med Cell Longev. 2017;2017:2712751. doi: 10.1155/2017/2712751. Epub 2017 May 14.
Oxidative states exert a significant influence on a wide range of biological and molecular processes and functions. When their balance is shifted towards enhanced amounts of free radicals, pathological phenomena can occur, as the generation of reactive oxygen species (ROS) in tissue microenvironment or in the systemic circulation can be detrimental. Epidemic chronic diseases of western societies, such as cardiovascular disease, obesity, and diabetes correlate with the imbalance of redox homeostasis. Current advances in our understanding of epigenetics have revealed a parallel scenario showing the influence of oxidative stress as a major regulator of epigenetic gene regulation via modification of DNA methylation, histones, and microRNAs. This has provided both the biological link and a potential molecular explanation between oxidative stress and cardiovascular/metabolic phenomena. Accordingly, in this review, we will provide current insights on the physiological and pathological impact of changes in oxidative states on cardiovascular disorders, by specifically focusing on the influence of epigenetic regulation. A special emphasis will highlight the effect on epigenetic regulation of human's current life habits, external and environmental factors, including food intake, tobacco, air pollution, and antioxidant-based approaches. Additionally, the strategy to quantify oxidative states in humans in order to determine which biological marker could best match a subject's profile will be discussed.
氧化状态对广泛的生物和分子过程及功能产生重大影响。当它们的平衡朝着自由基数量增加的方向转变时,就可能出现病理现象,因为组织微环境或体循环中活性氧(ROS)的产生可能是有害的。西方社会的流行性慢性病,如心血管疾病、肥胖症和糖尿病,都与氧化还原稳态的失衡有关。我们目前对表观遗传学的理解进展揭示了一种类似的情况,即氧化应激作为表观遗传基因调控的主要调节因子,通过修饰DNA甲基化、组蛋白和微小RNA发挥影响。这为氧化应激与心血管/代谢现象之间提供了生物学联系和潜在的分子解释。因此,在本综述中,我们将通过特别关注表观遗传调控的影响,提供关于氧化状态变化对心血管疾病生理和病理影响的当前见解。特别强调将突出人类当前生活习惯、外部和环境因素(包括食物摄入、烟草、空气污染和基于抗氧化剂的方法)对表观遗传调控的影响。此外,还将讨论量化人类氧化状态以确定哪种生物标志物最能匹配个体特征的策略。