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Despite their heterogeneous clinical manifestations, these conditions represent a continuum from acute adaptive stress to chronic maladaptive compensation, unified by persistent oxygen deprivation and dysregulated systemic homeostasis. G protein\u2010coupled receptors (GPCRs), the largest superfamily of membrane receptors, have emerged as central regulators of hypoxia sensing, ventilatory control, vascular tone, barrier integrity, erythropoiesis, immune activation, and metabolic reprogramming. However, how specific GPCR subtypes and their downstream signaling networks coordinate adaptation versus maladaptation across distinct organ systems and disease stages remains incompletely defined. This review synthesizes recent mechanistic insights into GPCR\u2010mediated pathways that govern neural, pulmonary, vascular, and hematologic responses to hypoxia. We examine the transition from protective to pathological signaling, highlight receptor\u2010level divergence that enables therapeutic selectivity, and evaluate translational prospects for GPCR\u2010targeted strategies, including biased agonism, receptor\u2010specific modulation, and sex\u2010based interventions. 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