Carbon monoxide and mitochondria: Cell energy and fate control.

Carbon monoxide (CO) is a ubiquitously produced endogenous gas in mammalian cells and is involved in stress response being considered as a cytoprotective and homeostatic factor. In the present review, the underlying mechanisms of CO are discussed, in particular CO's impact on cellular metabolism affecting cell fate and function. One of the principal signaling molecules of CO is reactive oxygen species (ROS), particularly hydrogen peroxide, which is mainly generated at the mitochondrial level. Likewise, CO acts on mitochondria modulating oxidative phosphorylation and mitochondria quality control, namely mitochondrial biogenesis (mitobiogenesis) and mitophagy. Other metabolic pathways are also involved in CO's mode of action such as glycolysis and pentose phosphate pathway. The review ends with some new perspectives on CO Biology research. Carboxyhemoglobin (COHb) formation can also be implicated in the CO mode of action, as well as its potential biological role. Finally, other organelles such as peroxisomes hold the potential to be targeted and modulated by CO.