Key result
Genetic mutations in cardiac ion channels, serotonin, and metabolic pathways are linked to SIDS risk.
Why the study?
Sudden infant death syndrome remains a leading cause of infant mortality in developed countries, but its underlying mechanisms remain largely unclear.
This narrative review highlights the multifactorial genetic basis of SIDS, including cardiac ion channel mutations, to improve risk assessment and targeted interventions.
May support genetic counseling after SIDS; extends multifactorial risk evidence and leaves open optimal screening protocols.
Sudden Infant Death Syndrome (SIDS) continues to be one of the most challenging and tragic causes of infant mortality in developed countries. While public health interventions have reduced its prevalence, the underlying mechanisms contributing to SIDS remain largely unclear. The biological basis of SIDS is widely believed to be multifactorial in nature, involving inherited genetic vulnerabilities, including mutations in cardiac ion channels and genes associated with brainstem serotonin function, metabolic enzymes, and inflammatory mediators. This review presents a comprehensive analysis of genetic studies relating to SIDS, incorporating recent findings from molecular autopsies, genome-wide association studies and functional assays. It also explores how gene–environment interactions, polygenic risk scores, and multi-omic strategies are reshaping our understanding of this complex condition. The review aims to integrate recent insights from molecular autopsy, genomic profiling, and gene–environment interactions to offer a framework for better risk assessment and the stratification of vulnerable infants who could benefit from targeted clinical and public health interventions.
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Rao et al. (2026) studied this question. Genetic mutations in cardiac ion channels, serotonin pathways, metabolic enzymes, and inflammation contribute to SIDS risk, aiding future risk assessment and interventions.
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