Senderovic Admina, Galijasevic Semira
Public Institution of Health Centers of the Canton of Sarajevo, Laboratory Diagnostics Service of the Ilidza, Health Center, Ilidza, Bosnia and Herzegovina.
Sarajevo Medical School, University Sarajevo School of Science and Technology, Sarajevo, Bosnia and Hercegovina.
Cardiol Res. 2024 Oct;15(5):330-339. doi: 10.14740/cr1700. Epub 2024 Oct 11.
Chronic coronary syndrome (CCS) is a long-term manifestation of coronary artery disease, marked by stable but recurring chest pain and myocardial ischemia due to the gradual buildup of atherosclerotic plaques in the coronary arteries. It is a metabolic disorder of coronary arteries characterized by oxidative stress, endothelial dysfunction, inflammation, and hyperlipidemia. The imbalance in oxidative-antioxidative status contributes to stable ischemic heart disease. Oxidative stress involves reactive oxygen and nitrogen species, leading to low-density lipoprotein (LDL) oxidation. Endothelial dysfunction, marked by reduced nitric oxide (NO) bioavailability, is an early onset of CCS, affecting vasodilation, cell proliferation, and inflammatory responses. Enzyme myeloperoxidase (MPO), traditionally considered protective, plays a dual role in initiating and progressing inflammatory diseases. MPO interacts with NO, modulating its catalytic activity. Elevated NO levels inhibit MPO through a reversible complex formation, preventing NO-induced inhibition by inducible nitric oxide synthase (iNOS). MPO also inactivates endothelial nitric oxide synthase (eNOS) and reacts with L-arginine, hindering NO synthesis. The interplay between MPO and NO significantly influences inflammation sites, impacting peroxidation rates and oxidation reactions. Peroxynitrite, a reactive species, contributes to nitration of tyrosine residues and lipid peroxidation. Mechanistic pathways suggest MPO enhances iNOS catalytic activity, influencing CCS development. iNOS, implicated in inflammation and atherosclerosis, is connected to NO regulation. This review analyzes the complex interplay of MPO, iNOS, and NO that affects plaque morphology, oxidative stress, and inflammation, contributing to atherosclerosis progression. Therefore, it is possible that the phenotypes of atherosclerotic plaques, focal and diffuse coronary artery disease, could be defined by the relationship between MPO and iNOS.
慢性冠状动脉综合征（CCS）是冠状动脉疾病的一种长期表现，其特征为由于冠状动脉中动脉粥样硬化斑块逐渐形成而导致的稳定但反复发作的胸痛和心肌缺血。它是一种冠状动脉的代谢紊乱，其特征为氧化应激、内皮功能障碍、炎症和高脂血症。氧化-抗氧化状态的失衡导致稳定型缺血性心脏病。氧化应激涉及活性氧和氮物种，导致低密度脂蛋白（LDL）氧化。以一氧化氮（NO）生物利用度降低为特征的内皮功能障碍是CCS的早期表现，影响血管舒张、细胞增殖和炎症反应。传统上被认为具有保护作用的髓过氧化物酶（MPO）在炎症性疾病的发生和发展中起双重作用。MPO与NO相互作用，调节其催化活性。NO水平升高通过形成可逆复合物抑制MPO，防止诱导型一氧化氮合酶（iNOS）对NO的抑制。MPO还使内皮型一氧化氮合酶（eNOS）失活，并与L-精氨酸反应，阻碍NO的合成。MPO与NO之间的相互作用显著影响炎症部位，影响过氧化速率和氧化反应。过氧亚硝酸盐是一种活性物质，有助于酪氨酸残基的硝化和脂质过氧化。机制途径表明MPO增强iNOS催化活性，影响CCS的发展。iNOS与炎症和动脉粥样硬化有关，与NO调节有关。本综述分析了影响斑块形态、氧化应激和炎症的MPO、iNOS和NO之间的复杂相互作用，促进了动脉粥样硬化的进展。因此，动脉粥样硬化斑块的表型，即局灶性和弥漫性冠状动脉疾病，有可能由MPO和iNOS之间的关系来定义。
