Obstructive sleep apnoea and cardiovascular consequences: Pathophysiological mechanisms.

Area of Science:

• Cardiovascular Science
• Metabolic Science
• Sleep Medicine

Background:

• Obstructive sleep apnoea (OSA) is a global health issue affecting nearly one billion people.
• OSA is an independent cardiovascular risk factor linked to obesity, insulin resistance, hypertension, and heart failure.
• Current treatment, continuous positive airway pressure, improves symptoms but has limited impact on comorbidities.

Purpose of the Study:

• To review molecular pathways, cellular, and tissue interactions in the cardiometabolic consequences of intermittent hypoxia.
• To identify potential pharmacological targets for OSA-related comorbidities.
• To explore the role of hypoxia-inducible factor-1 and mitochondrial dysfunction.

Main Methods:

• Review of experimental settings involving intermittent hypoxia in cells, rodents, and humans.
• Analysis of molecular pathways triggered by intermittent hypoxia.
• Examination of cellular and tissue interactions contributing to cardiometabolic dysfunction.

Main Results:

• Intermittent hypoxia triggers sympathetic activation, low-grade inflammation, oxidative stress, and endoplasmic reticulum stress.
• These pathways contribute to cardiometabolic dysfunction in OSA.
• Hypoxia-inducible factor-1 plays a key role, alongside significant mitochondrial functional changes.

Conclusions:

• Understanding molecular pathways of intermittent hypoxia is crucial for developing new therapies for OSA comorbidities.
• Targeting pathways like inflammation, oxidative stress, and mitochondrial function may offer alternative or supplementary treatments to continuous positive airway pressure.
• Further research into hypoxia-inducible factor-1 and mitochondrial dynamics is warranted.