Department of Surgery and Pediatrics, Drexel University College of Medicine, Philadelphia, PA, USA.
Med Gas Res. 2020 Jan-Mar;10(1):37-46. doi: 10.4103/2045-9912.279982.
Nitric oxide, studied to evaluate its role in cardiovascular physiology, has cardioprotective and therapeutic effects in cellular signaling, mitochondrial function, and in regulating inflammatory processes. Heme oxygenase (major role in catabolism of heme into biliverdin, carbon monoxide (CO), and iron) has similar effects as well. CO has been suggested as the molecule that is responsible for many of the above mentioned cytoprotective and therapeutic pathways as CO is a signaling molecule in the control of physiological functions. This is counterintuitive as toxic effects are related to its binding to hemoglobin. However, CO is normally produced in the body. Experimental evidence indicates that this toxic gas, CO, exerts cytoprotective properties related to cellular stress including the heart and is being assessed for its cytoprotective and cytotherapeutic properties. While survival of adult cardiomyocytes depends on oxidative phosphorylation (survival and resulting cardiac function is impaired by mitochondrial damage), mitochondrial biogenesis is modified by the heme oxygenase-1/CO system and can result in promotion of mitochondrial biogenesis by associating mitochondrial redox status to the redox-active transcription factors. It has been suggested that the heme oxygenase-1/CO system is important in differentiation of embryonic stem cells and maturation of cardiomyocytes which is thought to mitigate progression of degenerative cardiovascular diseases. Effects on other cardiac cells are being studied. Acute exposure to air pollution (and, therefore, CO) is associated with cardiovascular mortality, myocardial infarction, and heart failure, but changes in the endogenous heme oxygenase-1 system (and, thereby, CO) positively affect cardiovascular health. We will review the effect of CO on heart health and function in this article.
一氧化氮（NO）是一种在心血管生理学中被研究的物质，它在细胞信号转导、线粒体功能和炎症过程调节中具有心脏保护和治疗作用。血红素加氧酶（HO）在血红素代谢为胆红素、一氧化碳（CO）和铁方面起着主要作用，也具有类似的作用。CO 被认为是许多上述细胞保护和治疗途径的分子，因为 CO 是控制生理功能的信号分子。这是违反直觉的，因为毒性作用与它与血红蛋白的结合有关。然而，CO 通常在体内产生。实验证据表明，这种有毒气体 CO 发挥细胞保护特性与细胞应激有关，包括心脏，并正在评估其细胞保护和细胞治疗特性。虽然成年心肌细胞的存活依赖于氧化磷酸化（生存和由此导致的心脏功能受损是由线粒体损伤引起的），但线粒体生物发生被血红素加氧酶-1/CO 系统改变，并且可以通过将线粒体氧化还原状态与氧化还原活性转录因子相关联来促进线粒体生物发生。有人认为，血红素加氧酶-1/CO 系统在胚胎干细胞的分化和心肌细胞的成熟中很重要，这被认为可以减轻退行性心血管疾病的进展。其他心脏细胞的影响正在研究中。急性暴露于空气污染（因此包括 CO）与心血管死亡率、心肌梗死和心力衰竭有关，但内源性血红素加氧酶-1 系统（因此包括 CO）的变化对心血管健康有积极影响。我们将在本文中综述 CO 对心脏健康和功能的影响。
