Molecular Signaling and Plasticity in Carotid Body Type II Cells: From Purinergic Communication to Neurogenic Regulation

Carotid body type II cells constitute a glial-like cellular compartment with emerging molecular roles in intercellular signaling and adaptive plasticity. This narrative review critically examines the molecular mechanisms underlying type II-cell function, with particular emphasis on purinergic and non-purinergic signaling pathways. It also addresses the expression of sensory ion channels and the molecular regulation of the adult carotid body neurogenic niche. Functional studies in rats demonstrate adenosine triphosphate-induced intracellular calcium mobilization and secondary nucleotide release, whereas studies in human tissues demonstrate the immunohistochemical expression of signaling proteins and ion channels in identified cell populations, without establishing their functional activity. Glial fibrillary acidic protein-positive progenitor cells contribute to hypoxia-induced carotid body growth, alongside the recruitment of lineage-committed neuroblasts and expansion within the type I-cell lineage. The relative contributions of these populations vary across experimental models. Aging and disease observations identify candidate molecular changes but rarely establish type II-cell-specific causality. The central challenge is to link molecular identity, functional signaling, and lineage potential within defined cell populations, particularly in human tissue.