Clonal Hematopoiesis of Indeterminate Potential With Loss of < em > Tet2 < /em > Enhances Risk for Atrial Fibrillation Through < em > Nlrp3 < /em > Inflammasome Activation

CONCLUSIONS: We identified a modest association between CHIP, particularly TET2 CHIP, and incident AF in the UK Biobank population. In a mouse model of AF resulting from hematopoietic-specific inactivation of Tet2, we propose altered calcium handling as an arrhythmogenic mechanism, dependent on Nlrp3 inflammasome activation. Our data are in keeping with previous studies of CHIP in cardiovascular disease, and further studies into the therapeutic potential of NLRP3 inhibition for individuals with TET2 CHIP may be warranted.PMID:38357791 | DOI:10.1161/CIRCULATIONAHA.123.065597

Source: Circulation - February 15, 2024 Category: Cardiology Authors: Amy Erica Lin Aneesh C Bapat Ling Xiao Abhishek Niroula Jianchuan Ye Waihay J Wong Mridul Agrawal Christopher J Farady Andreas Boettcher Christopher B Hergott Marie McConkey Patricio Flores-Bringas Veronica Shkolnik Alexander G Bick David Milan Pradeep Na Source Type: research