Recent Advances in Studies on the Role of Neuroendocrine Disorders in Obstructive Sleep Apnea-Hypopnea

Wanda Wang1, Yanli Zheng1, Meimei Li1

  • 1Department of Cardiology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, People's Republic of China.

Insights

Obstructive sleep apnea-hypopnea syndrome (OSAHS) contributes to atherosclerosis (AS) by affecting the nervous system. This review explores neuroendocrine dysfunction as a key mechanism linking OSAHS to AS development.

Area of Science:

  • Cardiovascular Science
  • Sleep Medicine
  • Neuroendocrinology

Background:

  • Atherosclerosis (AS) and obstructive sleep apnea-hypopnea syndrome (OSAHS) are significant contributors to global cardiovascular disease mortality.
  • OSAHS is known to induce endothelial injury, vascular smooth muscle cell proliferation, dyslipidemia, and hypertension, but the precise mechanisms driving AS remain elusive.
  • The nervous system plays a crucial role in regulating metabolic and inflammatory processes implicated in AS pathogenesis.

Purpose of the Study:

  • To review the potential mechanisms of neuroendocrine disorders in the development of OSAHS-induced atherosclerosis.
  • To provide a foundation for developing targeted intervention strategies for OSAHS-related cardiovascular complications.

Main Methods:

  • Literature review focusing on the interplay between the nervous system, neuroendocrine function, and OSAHS.
  • Analysis of studies investigating neurophysiological changes and modulator release in OSAHS.
  • Synthesis of evidence linking neuroendocrine dysfunction to AS pathogenesis.

Main Results:

  • OSAHS can induce neurophysiological plasticity changes and alter modulator release, suggesting neuroendocrine dysfunction.
  • The nervous system's regulatory functions in appetite, metabolism, inflammation, oxidative stress, insulin resistance, and vasoconstriction are affected by OSAHS.
  • Neuroendocrine dysregulation is proposed as a critical pathway connecting OSAHS to the initiation and progression of AS.

Conclusions:

  • Neuroendocrine dysfunction is a plausible mechanism underlying OSAHS-induced atherosclerosis.
  • Understanding these neuroendocrine pathways offers new avenues for therapeutic interventions against AS in OSAHS patients.

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