Cellular Signaling Pathways and Atrial Remodeling in Atrial Fibrillation-Cellular Signaling Pathways and Atrial Remodeling in Atrial Fibrillation

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Video Summary

The session focused on cellular signaling pathways in atrial fibrillation (AF). Xun Ai from The Ohio State University discussed her research on MAP kinases, highlighting the roles of ERK, P38, and particularly JNK in AF development. She found that JNK activation is linked with aging-associated AF and binge alcohol exposure, influencing AF inducibility through cardiac stress conditions. The research also explored the roles of inflammatory cytokines and gastrointestinal dysfunction in promoting chronic inflammation, contributing to AF.<br /><br />Raelynn Mo from UMass discussed calcineurin and NFAT signaling in AF, highlighting calcineurin's role in AF-induced remodeling through increased calcium signaling. She developed a hypothesis that calcineurin inhibition might reduce AF remodeling, evidenced by improved cardiac rhythms and reduced apoptosis in her pig model, though calcineurin inhibition was linked to unexpected cardiac hypertrophy.<br /><br />Dr. Natel explored the JAK-STAT signaling pathway in AF. Using canine models, his team found involvement of the PDGF system and JAK-STAT in left atrial remodeling. Inhibition of these pathways prevented fibroblast collagen secretion, essential in fibrosis. Another study highlighted IL-6 signaling through STAT3 as crucial in post-operative AF, indicating potential therapeutic targets.<br /><br />Dr. Guy Salama, absent in person, presented recorded findings on Wnt canonical signaling and AF, suggesting relaxin's role in reversing AF and fibrosis in aged rats. Relaxin increased expression of sodium channels and gap junction proteins, reducing inflammation and macrophage infiltration, pointing to a novel therapeutic pathway. These studies collectively underscore the complexity of AF mechanisms and suggest multiple therapeutic targets.

Keywords

atrial fibrillation

cellular signaling

MAP kinases

calcineurin

JAK-STAT pathway

inflammation

cardiac remodeling

fibrosis

therapeutic targets