Key result
Alamandine reduces AF susceptibility and mitigates atrial electrophysiological and structural remodelling in preclinical hypoxia.
Why the study?
Chronic intermittent hypoxia in obstructive sleep apnoea is an independent risk factor for cardiovascular disease, and the molecular mechanisms of alamandine's protective effects in OSA-associated atrial fibrillation are unclear.
Does alamandine reduce susceptibility to hypoxia-induced atrial fibrillation in a rat model?
Does alamandine reduce susceptibility to hypoxia-induced atrial fibrillation in a rat model?
Alamandine demonstrates potential as an anti-arrhythmic agent for hypoxia-induced atrial fibrillation by mitigating endoplasmic reticulum stress and pyroptosis pathways in a preclinical model.
Chronic intermittent hypoxia (CIH) constitutes the primary pathophysiological disturbance in obstructive sleep apnoea (OSA), recognised as an independent risk factor for cardiovascular disease. The protective peptide alamandine (ALA), emerging as a novel component of the renin-angiotensin system, holds potential for elucidating molecular mechanisms underlying OSA-associated atrial fibrillation (AF). This study demonstrates that ALA treatment downregulates the expression of molecules associated with the GRP78/ATF6/CHOP pathway and pyroptosis-related proteins, while simultaneously mitigating atrial electrophysiological and structural remodelling and reducing susceptibility to AF. These findings suggest that the cardioprotective effects of ALA may be mediated through regulation of ERS and pyroptosis-related pathways, providing preliminary experimental evidence for its potential application in AF therapy. However, the precise molecular mechanisms require further functional validation.
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Yang et al. (2026) studied Hypoxia-Induced Atrial Fibrillation. Alamandine (ALA) was evaluated on Susceptibility to atrial fibrillation and atrial electrophysiological and structural remodelling. Alamandine treatment reduced susceptibility to atrial fibrillation and mitigated atrial electrophysiological and structural remodelling in rats exposed to chronic intermittent hypoxia.
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