Genomic risk factors in sudden infant death syndrome

被引：0
作者：
David W Van Norstrand
Michael J Ackerman
机构：
[1] Mayo Clinic,Department of Molecular Pharmacology and Experimental Therapeutics
[2] Mayo Clinic,Departments of Medicine and Pediatrics, Divisions of Cardiovascular Diseases and Pediatric Cardiology, and the Windland Smith Rice Sudden Death Genomics Laboratory
来源：
Genome Medicine | / 2卷
关键词：
Sudden Infant Death Syndrome; Brugada Syndrome; Catecholaminergic Polymorphic Ventricular Tachycardia; Sudden Infant Death Syndrome Case; Cardiac Sodium Channel;
D O I：
暂无
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摘要：
Sudden infant death syndrome (SIDS) is a major contributor to postneonatal infant death, and is the third leading cause of infant mortality in the USA. While public health efforts have reduced these deaths in recent years, the pathogenesis of SIDS remains unclear. Epidemiological data on SIDS-related deaths have suggested genetic factors, and many studies have attempted to identify SIDS-associated genes. This has resulted in a large body of literature implicating various genes and their encoded proteins and signaling pathways in numerous cohorts of various sizes and ethnicities. This review has undertaken a systematic evaluation of these studies, identifying the pathways that have been implicated in these studies, including central nervous system pathways, cardiac channelopathies, immune dysfunction, metabolism/energy pathways, and nicotine response. This review also explores how new genomic techniques will aid in advancing our knowledge of the genomic risk factors associated with SIDS, including SNPs and copy number variation. Last, this review explores how the current information can be applied to aid in our assessment of the at risk infant population.
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