Carbon monoxide (CO) is a gasotransmitter endogenously produced by the activity of heme oxygenase, which is a stress-response enzyme. Endogenous CO or low concentrations of exogenous CO have been described to present several cytoprotective functions: anti-apoptosis, anti-inflammatory, vasomodulation, maintenance of homeostasis, stimulation of preconditioning and modulation of cell differentiation. The present review revises and discuss how CO regulates cell metabolism and how it is involved in the distinct cytoprotective roles of CO. The first found metabolic effect of CO was its increase on cellular ATP production, and since then much data have been generated. Mitochondria are the most described and studied cellular targets of CO. Mitochondria exposure to this gasotransmitter leads several consequences: ROS generation, stimulation of mitochondrial biogenesis, increased oxidative phosphorylation or mild uncoupling effect. Likewise, CO negatively regulates glycolysis and improves pentose phosphate pathway. More recently, CO has also been disclosed as a regulating molecule for metabolic diseases, such as obesity and diabetes with promising results.

一氧化碳 (CO) 是由血红素加氧酶（一种应激反应酶）的活性内源性产生的气体递质。内源性 CO 或低浓度的外源性 CO 已被描述为具有多种细胞保护功能：抗凋亡、抗炎、血管调节、维持稳态、刺激预处理和调节细胞分化。本综述修订并讨论了 CO 如何调节细胞代谢，以及它如何参与 CO 独特的细胞保护作用。 首先发现的 CO 代谢作用是它增加细胞 ATP 的产生，从那时起，已经产生了大量数据。线粒体是 CO 被描述和研究最多的细胞靶标。线粒体暴露于这种气体递质会导致多种后果：ROS 的产生、线粒体生物合成的刺激、氧化磷酸化的增加或轻微的解偶联效应。同样，CO 负向调节糖酵解并改善磷酸戊糖途径。最近，CO 也被披露为代谢疾病（例如肥胖症和糖尿病）的调节分子，并取得了有希望的结果。