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首页> 外文期刊>American Journal of Physiology >Carbon monoxide in lung cell physiology and disease
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Carbon monoxide in lung cell physiology and disease

机译：肺细胞生理和疾病中的一氧化碳

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Carbon monoxide (CO) is an endogenously produced gas that has gained recognition as a biological signal transduction effector with properties similar, but not identical, to that of nitric oxide (NO). CO, which binds primarily to heme iron, may activate the hemoprotein guanylate cyclase, although with lower potency than NO. Furthermore, CO can modulate the activities of several cellular signaling molecules such as p38 MAPK, ERK1/2, JNK, Akt, NF-kB, and others. Emerging studies suggest that mitochondria, the energy-generating organelle of cells, represent a key target of CO action in eukaryotes. Dose-dependent modulation of mitochondrial function by CO can result in alteration of mitochondrial membrane potential, mitochondrial reactive oxygen species production, release of proapoptotic and proinflammatory mediators, as well as the inhibition of respiration at high concentration. CO, through modulation of signaling pathways, can impact key biological processes including autophagy, mitochondrial biogenesis, programmed cell death (apoptosis), cellular proliferation, inflammation, and innate immune responses. Inhaled CO is widely known as an inhalation hazard due to its rapid complexation with hemoglobin, resulting in impaired oxygen delivery to tissues and hypoxemia. Despite systemic and cellular toxicity at high concentrations, CO has demonstrated cyto- and tissue-protective effects at low concentration in animal models of organ injury and disease. These include models of acute lung injury (e.g., hyperoxia, hypoxia, ischemia-reperfusion, mechanical ventilation, bleomycin) and sepsis. The success of CO as a candidate therapeutic in preclinical models suggests potential clinical application in inflammatory and proliferative disorders, which is currently under evaluation in clinical trials.
机译：一氧化碳（CO）是内源性产生的气体，其具有与一氧化氮（NO）相似但不相同的具有相似但不相同的生物信号转导效应识别的气体。 CO，它主要与血红素铁结合，可以激活血蛋白胍基环化酶，尽管效率低于NO。此外，CO可以调节几种细胞信号分子的活性，例如P38 MAPK，ERK1 / 2，JNK，AKT，NF-KB等。新兴的研究表明，线粒体，细胞的能量产生细胞器，代表了真核生物中CO动作的关键目标。通过CO的线粒体功能的剂量依赖性调节可导致线粒体膜电位的改变，线粒体反应性氧物种生产，促孔和促炎介质的释放，以及高浓度的抑制。通过调制信号途径的CO，可以影响主要生物过程，包括自噬，线粒体生物发生，编程细胞死亡（细胞凋亡），细胞增殖，炎症和先天免疫应答。吸入的CO由于其与血红蛋白的快速络合而被广泛称为吸入危害，导致氧气输送受损到组织和低氧血症。尽管在高浓度下具有全身和细胞毒性，但CO已经在器官损伤和疾病的动物模型中表现出低浓度的细胞和组织保护作用。这些包括急性肺损伤的模型（例如，高氧，缺氧，缺血再灌注，机械通风，玻璃霉素）和败血症。 CO作为临床前模型的候选治疗的成功表明炎症和增殖性疾病中的潜在临床应用，目前正在评估临床试验。

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