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The Dual Role of Inducible Nitric Oxide Synthase in Myocardial Ischemia/Reperfusion Injury: Friend or Foe?

机译:诱导型一氧化氮合酶在心肌缺血/再灌注损伤中的双重作用:是敌是友?

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Nitric oxide synthases (NOSs) are a family of enzymes that are responsible for the synthesis of nitric oxide (NO) from the amino acid L-arginine in the body. Among the three key NOSs, the expression of inducible NOS (iNOS) can only be induced by inflammatory stimuli and contribute to the large amount of NO production. iNOS-derived NO plays an important role in various physiological and pathophysiological conditions, including the ischemic heart disease. Nowadays, the development of specific iNOS inhibitors and the availability of iNOS knockout mice have provided substantial evidence to support the role of iNOS/NO signaling in the myocardium. Nevertheless, the role of iNOS/NO signaling in the myocardial ischemic reperfusion injury is very complex and highly perplexing; both detrimental and beneficial effects of iNOS have been described. Thus, this review will aim at providing basic insights into the current progress of the role of iNOS in myocardial ischemia reperfusion injury. A better understanding of the dual role of iNOS in details may help facilitate the development of more effective therapies for the management of ischemic heart diseases.
机译:一氧化氮合酶(NOS)是一类酶,负责从体内的氨基酸L-精氨酸合成一氧化氮(NO)。在这三种主要的NOS中,诱导型NOS(iNOS)的表达只能通过炎症刺激来诱导,并有助于大量NO的产生。 iNOS衍生的NO在各种生理和病理生理状况(包括缺血性心脏病)中起着重要作用。如今,特定iNOS抑制剂的开发和iNOS基因敲除小鼠的可用性为支持iNOS / NO信号在心肌中的作用提供了大量证据。然而,iNOS / NO信号在心肌缺血再灌注损伤中的作用非常复杂且令人困惑。已经描述了iNOS的有害作用和有益作用。因此,本综述旨在提供有关iNOS在心肌缺血再灌注损伤中作用的最新进展的基本见解。更好地了解iNOS的双重作用可能有助于促进开发更有效的方法来治疗缺血性心脏病。

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