Authors:

Prisha Pandita

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Atrial fibrillation (AF) represents one of the most common arrhythmias seen clinically and is associated with a significant increase in morbidity and mortality. One of the main contributors to the pathophysiology for the initiation, progression, and persistence of AF is inflammation. Inflammatory infiltrates and increased serum levels of proinflammatory cytokines have been demonstrated in animal models and patients with AF. AF progression is associated with increased levels of these pro- inflammatory cytokines. Cigarette smoking is associated with an increased risk of AF. Moreover, cigarette smoke is known to increase inflammation and pro-inflammatory cytokines including interleukin (IL)-1β, IL-18, and tumor necrosis factor-α (TNF- α).Therefore, it is of great clinical importance to elucidate the underlying mechanisms contributing to smoking induced inflammation in AF patients. A critical amplifier of inflammation is the NLRP3 inflammasome, which is increased in patients with AF. Here, we identify critical upstream mechanisms leading to NLRP3 inflammasome activation via endoplasmic reticulum (ER) stress in atrial tissues from AF patients and human induced pluripotent stem cell-atrial cardiomyocytes. These findings reveal important mechanistic insights into possible upstream targets in controlling excessive inflammation due to smoking in AF patients. Developing Anti-Racist Curricula: A Case Study on ADHD in Black Youth Ethan Pang

Source:

UC Davis / MED: Int Med Cardiology (davis) / 2025

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Co-authors:

Prisha Pandita