Key result
ALDH2 activation and ALDH2 activators show potential antiarrhythmic benefits, whereas the ALDH2*2 polymorphism (rs671) is associated with increased arrhythmic risk.
Why the study?
Despite remarkable progress, antiarrhythmic therapy remains suboptimal, while accumulating evidence indicates ALDH2 activation has potential antiarrhythmic benefits.
Does ALDH2 activation provide antiarrhythmic protection in individuals at risk of cardiac arrhythmia?
Does ALDH2 activation provide antiarrhythmic protection in individuals at risk of cardiac arrhythmia?
ALDH2 activation represents a promising potential therapeutic strategy for antiarrhythmic protection.
ALDH2 modulation merits prospective trials as antiarrhythmic strategy; leaves open clinical translation of activators or rs671 genotyping.
Cardiac arrhythmia is a common cardiovascular disease that leads to considerable economic burdens and significant global public health challenges. Despite the remarkable progress made in recent decades, antiarrhythmic therapy remains suboptimal. Aldehyde dehydrogenase 2 (ALDH2), a critical detoxifying enzyme, catalyzes toxic aldehydes and protects individuals from damage caused by oxidative stress. Accumulating evidence has demonstrated that ALDH2 activation has potential antiarrhythmic benefits. The correlation between ALDH2 deficiency and arrhythmogenesis has been widely recognized. In this review, we summarize recent research on the potential role of ALDH2 activation and antiarrhythmic protection, as well as the role played by the ALDH2∗2 polymorphism (rs671) in promoting arrhythmic risk. Additionally, we discuss important new findings illustrating the use of ALDH2 activators, which may prove to be promising antiarrhythmic therapy agents.
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Jin et al. (2022) conducted a review in Cardiac arrhythmia. ALDH2 activation and ALDH2 activators was evaluated. ALDH2 activation and ALDH2 activators show potential antiarrhythmic benefits, whereas the ALDH2*2 polymorphism (rs671) is associated with increased arrhythmic risk.
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