This review explores the mechanisms, complications, and evolving management of obstructive sleep apnea, suggesting the importance of a fibrosis-linked perspective.
Obstructive sleep apnea (OSA) is a highly prevalent yet substantially underdiagnosed sleep‐related breathing disorder increasingly recognized as a heterogeneous systemic disease rather than a purely mechanical consequence of recurrent upper‐airway collapse. This review provides an updated and integrated overview of OSA, spanning epidemiology, multifactorial pathophysiology, heterogeneous clinical presentation, major cardiometabolic and end‐organ consequences, diagnostic principles, and evolving personalized management, while also emphasizing the limitations of conventional severity classification, which is predominantly based on the apnea–hypopnea index. We highlight how intermittent hypoxia–reoxygenation, sleep fragmentation, sympathetic activation, intrathoracic pressure stress, endothelial dysfunction, inflammation, oxidative stress, and metabolic dysregulation interact to drive systemic injury, and why physiologically enriched metrics such as hypoxic burden, T90, event duration, sleep‐stage dependency, and endotypic heterogeneity may better capture biological risk than event frequency alone. Within this broader framework, fibrosis‐linked structural remodeling emerges as an important yet under‐supported dimension of OSA pathobiology. Experimental and clinical evidence suggests that OSA may contribute to remodeling of the lungs, liver, kidneys, and heart, although the strength of the evidence and the degree of causal inference vary across organs. By integrating established knowledge with this emerging fibrosis‐oriented perspective, this review defines key mechanistic, diagnostic, and translational priorities for future research and phenotype‐aware clinical stratification.
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Thuy et al. (2026) studied this question.
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