Key result
The rs11667393 variant in the TRPM4 gene was nominally associated with an increased risk of sudden infant death syndrome (OR 1.438), though significance was lost after correction for multiple testing.
Why the study?
Brain edema and cerebral water channel gene variants may play a role in SIDS pathogenesis, prompting investigation into whether SUR1-TRPM4 channel complex variants are linked to SIDS.
Are genetic variants in the SUR1-TRPM4 non-selective cation channel associated with an increased risk of sudden infant death syndrome (SIDS)?
Case-Control (n=524)
Are genetic variants in the SUR1-TRPM4 non-selective cation channel associated with an increased risk of sudden infant death syndrome (SIDS)?
Variants in the SUR1-TRPM4 channel complex showed nominal associations with SIDS, suggesting a potential genetic role in cerebral edema, though findings require validation in larger cohorts.
Increasing evidence suggests that brain edema might play an important role in the pathogenesis of sudden infant death syndrome (SIDS) and that variants of genes for cerebral water channels might be associated with SIDS. The role of the sulfonylurea receptor 1 (SUR1)-transient receptor potential melastatin 4 (TRPM4) non-selective cation channel in cerebral edema was demonstrated by extensive studies. Therefore, we hypothesized that variants at genes of the SUR1-TRPM4 channel complex might be linked to SIDS. Twenty-four polymorphisms in candidate genes involved in the SUR1-TRPM4 non-selective cation channel were investigated in 185 SIDS cases and 339 controls. One (rs11667393 in TRPM4) of these analyzed SNPs reached nominal significance regarding an association with SIDS in the overall analysis (additive model: p = 0.015, OR = 1.438, 95% CI = 1.074-1.925; dominant model: p = 0.036; OR = 1.468, 95% CI = 1.024-2.106). In the stratified analysis, further 8 variants in ABCC8 (encoding SUR1) or TRPM4 showed pronounced associations. However, none of the results remained significant after correction for multiple testing. This preliminary study has provided the first evidence for a genetic role of the SUR1-TRPM4 complex in the etiology of SIDS, and we suggest that our initial results should be evaluated by further studies.
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Qu et al. (2022) conducted a case-control in Sudden infant death syndrome (SIDS) (n=524). rs11667393 variant in the TRPM4 gene vs. Non-carriers / Controls was evaluated on Association of rs11667393 with SIDS (additive model) (OR 1.438, 95% CI 1.074-1.925, p=0.015). The rs11667393 variant in the TRPM4 gene was nominally associated with an increased risk of sudden infant death syndrome (OR 1.438), though significance was lost after correction for multiple testing.
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