Key result
Inflammation promotes AF via oxidative stress, autonomic imbalance, and structural changes, highlighting novel therapeutic targets.
Why the study?
Atrial fibrillation is the most common sustained cardiac arrhythmia and inflammation is linked to its pathogenesis, motivating an exploration of the underlying pathophysiological processes and novel therapeutic targets.
What are the pathophysiological processes linking inflammation to atrial fibrillation and what are potential novel therapeutic targets?
What are the pathophysiological processes linking inflammation to atrial fibrillation and what are potential novel therapeutic targets?
This review highlights the role of systemic and local inflammation in the pathogenesis of atrial fibrillation and identifies inflammatory pathways as potential therapeutic targets.
Answers are grounded in this paper and cite their sources.
Should not yet change AF practice; extends inflammatory mechanisms and identifies novel therapeutic targets for research.
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, and inflammation has been suggested as a predisposing factor for AF. Systemic inflammatory disorders (including autoimmune disorder, diabetes mellitus, and obesity) or local inflammation of the heart or pericardium are linked to AF. Inflammation is known to trigger various signalling pathways and to directly influence proinflammatory cytokines, in turn promoting structural and electrical changes in the atria, increasing the susceptibility to AF. Inflammation induces oxidative stress and an imbalance in the autonomic nervous system, and enhances atrial or pulmonary vein arrhythmogenesis by modulating electrophysiological characteristics and fibrogenesis. This review explores the complex pathophysiological processes linking inflammation to AF and identifies potential novel therapeutic targets.
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Lu et al. (2026) conducted a review in Atrial fibrillation. Inflammation promotes atrial fibrillation by inducing oxidative stress, autonomic imbalance, and structural changes, highlighting inflammatory pathways as potential novel therapeutic targets.
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