Targeting Ca2+-dependent arrhythmias and remodeling via inhibition of TRPC and endo-lysosomal channels
We will develop therapeutic strategies to target TRPC, ORAI and endo-lysosomal channels with small molecules and by base and prime editing approaches. In addition, Ca2+ channels and signaling pathways in macrophages contributing to cardiac remodeling through cardiocrine signaling will be identified.