JNK2 Is a Stress Integrator Driving Atrial Fibrillation Pathogenesis in Aging via Gut-Heart Crosstalk.

Jiajie Yan, Elena Carrillo, Aaryan Kohli, Saugat Khanal, Nikola Ricchiuti, Jaime DeSantiago, Xiaoping Wan, Mei Han, Abigail Richardson, Mei Yang, Jesus Rondon, Le Shen, Jun Sun, Qiangrong Liang, Thomas J Hund, Jarek Meller, Isabelle Deschenes, Dan J Bare, Xun Ai

Department of Physiology and Cell Biology (J.Y., A.K., S.K., N.R., X.W., A.R., I.D., D.J.B., X.A.), The Ohio State University, Columbus, OH.Department of Physiology and Cell Biology (J.Y., A.K., S.K., N.R., X.W., A.R., I.D., D.J.B., X.A.), The Ohio State University, Columbus, OH. · pubmed

Paper

Abstract

Atrial fibrillation (AF) is the most common arrhythmia and is associated with high morbidity and mortality, particularly in the aging population. Current treatment and prevention strategies remain suboptimal, highlighting the urgent need to better understand the mechanisms underlying aging-associated AF. We recently reported a causal role of the stress-activated kinase JNK2 (c-Jun N-terminal kinase 2) in aging-associated AF pathogenesis, mediated by JNK2-driven sarcoplasmic reticulum Ca

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Research summary

The paper claims that JNK2 is a key mediator in the pathogenesis of atrial fibrillation associated with aging through gut-heart interactions. This research is relevant as it explores a potential underlying mechanism of aging-related disease rather than merely addressing symptoms.

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