Na Li, Ph.D.
Na Li, Ph.D.
- Assistant Professor
Baylor College of Medicine
Houston, Texas United States
- To investigate novel molecular mechanisms underlying cardiac arrhythmias and cardiomyopathy.
Professional StatementCardiac arrhythmias severely affect the cardiac performance, and in some cases are lethal. Arrhythmias can result from dysfunctional ion channels located on the plasma membrane or abnormal intracellular calcium handling. Emerging evidence suggests that risk factors for arrhythmias, such as inflammation, obesity, hypertension, etc. can modify the function of cardiac ion channels and calcium handling proteins via transcriptional or posttranscriptional mechanisms. The goal of our research is to elucidate the mechanistic link between these risk factors and the pathophysiology of cardiac arrhythmias, in order to develop novel therapeutic targets for arrhythmic patients.
Currently, the lab is focusing on two research area: 1 ) inflammasome-mediated pathogenesis of atrial fibrillation, and 2) the role of FKBP5 in cardiac arrhythmia and cardiomyopathy. We employ multidisciplinary approaches including electrophysiological studies, biochemical and molecular biological studies, bioinformatics analyses, and transcriptomics studies, etc. and utilize genetically engineered mouse models and human cardiac samples in our projects.
The lab is funded by research grants from National Institutes of Health. The trainee also received the fellowship from American Heart Association.
- "Enhanced Cardiomyocyte NLRP3 Inflammasome Signaling Promotes Atrial Fibrillation.." Circulation. 2018 :
- "Cardiomyocyte Inflammasome Signaling in Cardiomyopathies and Atrial Fibrillation: Mechanisms and Potential Therapeutic Implications.." Front Physiol.. 2018 :
- "Identification of microRNA-mRNA dysregulations in paroxysmal atrial fibrillation.." Int J Cardiol.. 2015 :
- "Loss of microRNA-106b-25 cluster promotes atrial fibrillation by enhancing ryanodine receptor type-2 expression and calcium release.." Circ Arrhythm Electrophysiol.. 2014 :
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