The Role of Inducible Nitric Oxide Synthase in Assessing the Functional Level of Coronary Artery Lesions in Chronic Coronary Syndrome.

IF 1.4 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS
Cardiology Research Pub Date : 2024-10-01 Epub Date: 2024-10-11 DOI:10.14740/cr1700
Admina Senderovic, Semira Galijasevic
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引用次数: 0

Abstract

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.

诱导型一氧化氮合成酶在评估慢性冠状动脉综合征冠状动脉病变功能水平中的作用
慢性冠状动脉综合征(CCS)是冠状动脉疾病的一种长期表现,其特征是由于冠状动脉中的动脉粥样硬化斑块逐渐堆积而导致的稳定但反复发作的胸痛和心肌缺血。它是冠状动脉的一种代谢紊乱,以氧化应激、内皮功能障碍、炎症和高脂血症为特征。氧化-抗氧化状态的失衡导致缺血性心脏病的稳定。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)生物利用率降低为特征的内皮功能障碍是慢性缺血性心脏病的早期症状,会影响血管扩张、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扮演着双重角色。MPO 与 NO 相互作用,调节其催化活性。NO 水平升高会通过可逆复合物的形成抑制 MPO,阻止 NO 诱导的诱导型一氧化氮合酶(iNOS)的抑制作用。MPO 还会使内皮一氧化氮合酶(eNOS)失活,并与 L-精氨酸发生反应,阻碍一氧化氮的合成。MPO 和 NO 之间的相互作用会对炎症部位产生重大影响,影响过氧化率和氧化反应。过氧化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。机理途径表明,MPO 可增强 iNOS 的催化活性,影响 CCS 的发展。iNOS 与炎症和动脉粥样硬化有关,与 NO 的调节有关。本综述分析了 MPO、iNOS 和 NO 的复杂相互作用,它们影响斑块形态、氧化应激和炎症,从而导致动脉粥样硬化的发展。因此,动脉粥样硬化斑块、局灶性和弥漫性冠状动脉疾病的表型有可能由 MPO 和 iNOS 之间的关系来定义。
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来源期刊
Cardiology Research
Cardiology Research CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
2.50
自引率
0.00%
发文量
42
期刊介绍: Cardiology Research is an open access, peer-reviewed, international journal. All submissions relating to basic research and clinical practice of cardiology and cardiovascular medicine are in this journal''s scope. This journal focuses on publishing original research and observations in all cardiovascular medicine aspects. Manuscript types include original article, review, case report, short communication, book review, letter to the editor.
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