Related Experiment Video
Updated: Oct 25, 2025

Author Spotlight: Traditional Chinese Medicine for Sleep Disorders in Acute COPD — A Safe, Cost-Effective Approach
Published on: October 18, 2024
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.
Abstract:
Cardiovascular disease is a common cause of death worldwide, and atherosclerosis (AS) and obstructive sleep apnea-hypopnea syndrome (OSAHS) critically contribute to the initiation and progression of cardiovascular diseases. OSAHS promotes endothelial injury, vascular smooth muscle cell (VSMC) proliferation, abnormal lipid metabolism, and elevated arterial blood pressure. However, the exact OSAHS mechanism that causes AS remains unclear. The nervous system is widely distributed in the central and peripheral regions. It regulates appetite, energy metabolism, inflammation, oxidative stress, insulin resistance, and vasoconstriction by releasing regulatory factors and participates in the occurrence and development of AS. Studies showed that OSAHS can cause changes in neurophysiological plasticity and affect modulator release, suggesting that neuroendocrine dysfunction may be related to the OSAHS mechanism causing AS. In this article, we review the possible mechanisms of neuroendocrine disorders in the pathogenesis of OSAHS-induced AS and provide a new basis for further research on the development of corresponding effective intervention strategies.
More Related Videos
Related Concept Videos
Sleep Apnea
The condition is more prevalent among...
Coronary Artery Disease I: Introduction
Atherosclerosis IV: Nursing Management
Atherosclerosis I: Introduction
Disorders of the Autonomic Nervous System
Raynaud's disease, also known as Raynaud's...
Hypertension II: Pathophysiology

