ArticleJournal of cardiovascular translational research2026
Alamandine Attenuates Hypoxia-Induced Atrial Fibrillation in Rats: Involvement of Endoplasmic Reticulum Stress and Pyroptosis Pathways.
Article in Journal of cardiovascular translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
7 authors.
Funding
Abstract
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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Registered trials
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