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Updated: May 7, 2026
Murine Isolated Heart Model of Myocardial Stunning Associated with Cardioplegic Arrest
Published on: August 6, 2015
The paraventricular thalamic nucleus is involved in sleep-fragmentation-associated cardiac dysfunction after acute
Yakun Bo1, Yu-Ting Tseng2, Guanfei Su3
1Cardiac Pacing and Electrophysiology Department, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China; Xinjiang Key Laboratory of Cardiac Electrophysiology and Cardiac Remodeling, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China; CAS Key Laboratory of Brain Connectome and Manipulation, Shenzhen-Hong Kong Institute of Brain Science, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Background:
Sleep is essential for cardiac recovery after myocardial infarction (MI), but the impact of altered sleep architecture on repair remains unclear.
Objective:
To investigate how sleep fragmentation affects cardiac repair post-MI and identify underlying neural mechanisms.
Methods:
In a mouse model of MI, we assessed sleep patterns and cardiac function. An activity-dependent genetic labeling system in TRAP2 mice was used to identify brain regions involved in MI-induced sleep disturbances. Chemogenetic inhibition of glutamatergic neurons in the paraventricular thalamus (PVT) was performed to evaluate its role in sleep and cardiac regulation.
Results:
Increased non-rapid eye movement (NREM) sleep fragmentation was negatively associated with cardiac recovery. Inhibition of PVT glutamatergic activity reduced sleep fragmentation and significantly improved cardiac repair.
Conclusion:
Our findings highlight the importance of sleep continuity in post-MI healing and identify the PVT as a key neural regulator of sleep-cardiac interaction. Targeting this pathway may offer a novel therapeutic approach to enhance MI recovery.
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