I am a molecular pharmacologist, and my laboratory aims to understand the role of microRNAs in the gut-heart axis. As a doctoral fellow, I investigated mechanistic associations between metabolic disturbances and prostatic disorders. That research centered on identifying the mechanisms contributing to a high incidence of prostatic disorders in insulin-resistant patients with compensatory hyperinsulinemia. As a postdoctoral fellow, I explored interactions between the intestinal microbiota and microRNAs in vascular disorders. Specifically, I initiated the microbiome-miR research project and identified a unique mode of communication between microbiota and the host, involving remote regulation of miRs with functional implications. I also spearheaded a collaborative project to understand the role of sodium channel trafficking in cardiac arrhythmias. Currently, I am focusing on the role of the microbiota-miR interaction in heart failure. My laboratory identified that the cardiac upregulation of microRNA-204 during hypertrophic stress is a compensatory cardioprotective response. Its effects are mediated by inhibiting the maladaptive stretch signaling of the apelin-receptor. We provide the first evidence that the apelin receptor cellular trafficking per se and its regulation by miR-204, leading to a change in the signaling outcome of APJ.

We also identified that the gamma-peptide nucleic acid-based microRNA inhibition weakens many of the concerns associated with developing microRNA therapeutics (e.g., binding affinity, enzymatic degradation, and non-specific interaction with proteins). Based on the robust preliminary data, we think the gamma-peptide nucleic acid will be efficient in microRNA inhibition, safer for long-term use, and suitable for cardiometabolic disorders. In summary, the focus is on utilizing interdisciplinary expertise to tackle the real challenges in cardiovascular diseases.