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Overarching Research Interests
- Decoding Inflammatory Pathways in Cardiac Arrhythmias and Myopathies
- How Inter-Organ Crosstalk Fuels the Risk of Cardiac Arrhythmias
Our group was the first to establish a causal role for inflammasome signaling in the development of atrial fibrillation (AF) [Yao et al, Circulation, 2018].
As the most common arrhythmia in adults, AF is increasingly prevalent due to a range of risk factors. Our ongoing projects aim to elucidate the mechanistic links between AF pathophysiology and common contributors such as clonal hematopoiesis, liver disease, and aging.
We recently identified FK506-binding protein 5 (FKBP5) as a novel molecular contributor to atrial cardiomyopathy. Our ongoing studies are focused on delineating the role of FKBP5 across various cardiac cell types and its involvement in fibrotic and inflammatory remodeling.
Molecular mechanisms of cardiac conduction disorders (CCD):
In collaboration with Dr. Mihail Chelu, we employ mouse models and human biopsy samples to investigate the molecular mechanisms underlying various forms of cardiac conduction disease (CCD), including sinoatrial node dysfunction and atrioventricular (AV) block.
TANGO2-deficiency disorder (TDD) is a rare disorder caused by mutations in the TANGO2 gene. Affected individuals experience arrhythmias. The molecular mechanisms underlying the development of cardiac arrhythmias in the context of TDD remain elusive. Our goals are to understand the function of TANGO2 in cardiomyocytes and elucidate the molecular underpinnings of arrhythmia development in the Tango2 knockout mouse model.
Li lab is funded by research grants from the National Institutes of Health ( R01HL136389, R01HL163277, R01HL164838; PI: Li) and the American Heart Association.
For complete publication, please check the NCBI bibliography
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