| Literature DB >> 22704942 |
Ming-Jie Yuan1, He Huang, Cong-Xin Huang.
Abstract
Sudden cardiac death (SCD) is a major cause of morbidity and mortality in patients with coronary artery diseases and myocardial infarction (MI). Sympathetic stimulation and sympathetic neural remodeling are important in the generation of SCD in diseased heart. The balance of nerve growth factor (NGF) and semaphoring 3A determines the sympathetic innervation patterning. Recently studies showed that P75 neurotrophin receptor (P75 NTR) is the main receptor for NGF mediates sympathetic hyperinnervation in the heart, and also interacts with semaphoring 3A. Sympathetic axons lacking P75 NTR are more sensitive to semaphoring 3A in vitro than control neurons, resulting in decreased sympathetic innervation in the left ventricular subendocardium. P75 NTR(-/-) mice had increased sympathetic heterogeneity and more spontaneous ventricular arrhythmias. Based on current studies, we present a hypothesis that P75 NTR plays an important regulatory role in sudden cardiac after myocardial infarction and hope to find new therapeutic target for SCD.Entities:
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Year: 2012 PMID: 22704942 DOI: 10.1016/j.mehy.2012.05.035
Source DB: PubMed Journal: Med Hypotheses ISSN: 0306-9877 Impact factor: 1.538