Related Experiment Video For chronic intermittent hypoxia
Updated: May 10, 2025

Delivery of In Vivo Acute Intermittent Hypoxia in Neonatal Rodents to Prime Subventricular Zone-derived Neural Progenitor Cell Cultures
Published on: November 2, 2015
Chronic Intermittent Hypoxia-Induced Neural Injury: Pathophysiology, Neurodegenerative Implications, and Therapeutic
Nan-Nan Jia1,2, Meng-Fan Yao1,3, Chun-Xue Zhu1,2
1The Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, Jiangsu, China.
Abstract:
Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a sleep-related respiratory disorder that poses a global threat to human health. Chronic intermittent hypoxia (CIH) is its main pathological feature. With the advancements in medical research, the study of CIH-induced neural injury has gained increasing attention. Studies have shown that CIH can lead to or aggravate neuroinflammation and apoptosis by increasing blood-brain barrier (BBB) permeability, promoting oxidative stress, activating glial cells, and triggering multiple signaling pathways, ultimately resulting in neural injury. These processes contribute to the development of Alzheimer's disease, Parkinson's disease, and stroke. This review aims to summarize the progress in CIH-induced neural injury and explore various underlying mechanisms, with the goal of providing new insights for the development of therapeutic interventions targeting CIH-related neural damage.
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