da Costa Rafael M, Rodrigues Daniel, Pereira Camila A, Silva Josiane F, Alves Juliano V, Lobato Núbia S, Tostes Rita C
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, São Paulo, Brazil.
Special Academic Unit of Health Sciences, Federal University of Goiás, Jataí, Brazil.
Front Pharmacol. 2019 Apr 12;10:382. doi: 10.3389/fphar.2019.00382. eCollection 2019.
Free radicals act as secondary messengers, modulating a number of important biological processes, including gene expression, ion mobilization in transport systems, protein interactions and enzymatic functions, cell growth, cell cycle, redox homeostasis, among others. In the cardiovascular system, the physiological generation of free radicals ensures the integrity and function of cardiomyocytes, endothelial cells, and adjacent smooth muscle cells. In physiological conditions, there is a balance between free radicals generation and the activity of enzymatic and non-enzymatic antioxidant systems. Redox imbalance, caused by increased free radical's production and/or reduced antioxidant defense, plays an important role in the development of cardiovascular diseases, contributing to cardiac hypertrophy and heart failure, endothelial dysfunction, hypertrophy and hypercontractility of vascular smooth muscle. Excessive production of oxidizing agents in detriment of antioxidant defenses in the cardiovascular system has been described in obesity, diabetes mellitus, hypertension, and atherosclerosis. The transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2), a major regulator of antioxidant and cellular protective genes, is primarily activated in response to oxidative stress. Under physiological conditions, Nrf2 is constitutively expressed in the cytoplasm of cells and is usually associated with Keap-1, a repressor protein. This association maintains low levels of free Nrf2. Stressors, such as free radicals, favor the translocation of Nrf2 to the cell nucleus. The accumulation of nuclear Nrf2 allows the binding of this protein to the antioxidant response element of genes that code antioxidant proteins. Although little information on the role of Nrf2 in the cardiovascular system is available, growing evidence indicates that decreased Nrf2 activity contributes to oxidative stress, favoring the pathophysiology of cardiovascular disorders found in obesity, diabetes mellitus, and atherosclerosis. The present mini-review will provide a comprehensive overview of the role of Nrf2 as a contributing factor to cardiovascular risk in metabolic diseases.
自由基作为第二信使,调节许多重要的生物学过程,包括基因表达、转运系统中的离子动员、蛋白质相互作用和酶功能、细胞生长、细胞周期、氧化还原稳态等。在心血管系统中,自由基的生理性产生确保了心肌细胞、内皮细胞和相邻平滑肌细胞的完整性和功能。在生理条件下,自由基产生与酶促和非酶促抗氧化系统的活性之间存在平衡。自由基产生增加和/或抗氧化防御降低引起的氧化还原失衡在心血管疾病的发展中起重要作用,导致心脏肥大和心力衰竭、内皮功能障碍、血管平滑肌肥大和过度收缩。在肥胖、糖尿病、高血压和动脉粥样硬化中,已发现心血管系统中氧化剂过度产生而损害抗氧化防御。转录因子Nrf2(核因子红细胞2相关因子2)是抗氧化和细胞保护基因的主要调节因子,主要在氧化应激反应中被激活。在生理条件下,Nrf2在细胞质中组成性表达,通常与抑制蛋白Keap-1相关联。这种关联维持低水平的游离Nrf2。应激源,如自由基,有利于Nrf2易位至细胞核。核内Nrf2的积累使该蛋白能够与编码抗氧化蛋白的基因的抗氧化反应元件结合。尽管关于Nrf2在心血管系统中作用的信息很少,但越来越多的证据表明,Nrf2活性降低会导致氧化应激,有利于肥胖、糖尿病和动脉粥样硬化中发现的心血管疾病的病理生理学。本综述将全面概述Nrf2作为代谢性疾病心血管风险促成因素的作用。