ALDH2 mutation and CoQ10 impactsALDH2 deficiency induces atrial fibrillation through dysregulated cardiac sodium channel and mitochondrial bioenergetics: A multi-omics analysis.
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Our investigation centered around the effects of a genetic mutation in the ALDH2 enzyme, known as ALDH2*2, on the risk of developing atrial fibrillation (AF). We discovered that this mutation led to an increased incidence of AF in mice, accompanied by a decrease in the threshold for AF events compared to their non-mutant counterparts.
A key finding in our study was the alteration in signaling pathways related to retinoic acid, which impacted the expression of crucial sodium channels involved in heart rhythm. The reduced levels of these channels, specifically the SCN5A, raised concerns about their role in AF susceptibility.
We also conducted a multi-omics analysis that revealed disruptions in fatty acid metabolism and energy production within the mitochondria, leading to heightened oxidative stress. To counter these issues, we administered Coenzyme Q10, a well-known mitochondrial co-factor, to the mutant mice. Remarkably, this treatment offered protection against AF episodes.
By bridging our findings, we could see how Coenzyme Q10 may pave the way for personalized treatment options for individuals with the ALDH2*2 genotype at risk for AF, making it a potential game-changer in managing heart health.