Mitochondrial acute oxygen sensing and signaling

Abstract

Oxygen (O₂) is essential for life and therefore the supply of sufficient O₂ to the tissues is a major physiological challenge. In mammals, a deficit of O₂ (hypoxia) triggers rapid cardiorespiratory reflexes (e.g. hyperventilation and increased heart output) that within a few seconds increase the uptake of O₂ by the lungs and its distribution throughout the body. The prototypical acute O₂-sensing organ is the carotid body (CB), which contains sensory glomus cells expressing O₂-regulated ion channels. In response to hypoxia, glomus cells depolarize and release transmitters which activate afferent fibers terminating at the brainstem respiratory and autonomic centers. In this review, we summarize the basic properties of CB chemoreceptor cells and the essential role played by their specialized mitochondria in acute O₂ sensing and signaling. We focus on recent data supporting a "mitochondria-to-membrane signaling" model of CB chemosensory transduction. The possibility that the differential expression of specific subunit isoforms and enzymes could allow mitochondria to play a generalized adaptive O₂-sensing and signaling role in a wide variety of cells is also discussed.

Keywords: arterial chemoreceptors; carotid body; cell physiology; cute hypoxia; glomus cells; itochondria; mitochondrial subunit isoforms; o; xygen sensing.