Chandrasekar Bysani, DVM, PhD

University of Missouri – Columbia (MU)

My long-term research has focused on dissecting the molecular mechanisms involved in the initiation and progression of ischemic heart disease, pressure-overload hypertrophy, heart failure (HF) and atherosclerosis, so that novel therapeutic targets can be identified.

TRAF3IP2, a cytoplasmic adapter molecule and upstream regulator of IKK, JNK, and p38 MAPK, serves as a nodal point in the activation of various proinflammatory signaling pathways in CVD. We utilize cell type-specific gene deletion and overexpression models. Our goal is to identify small molecule or pharmacological inhibitors of TRAF3IP2.

Cardiac fibrosis is a progressive disease and contributes to diastolic dysfunction and HF development. We focus on delineating the role of Larp6 and its partners in cardiac fibrosis using genetic and interventional models.

RECK, a MMP inhibitor, is significantly suppressed in failing human and mouse hearts. Our goal is to identify small molecule/pharmacological RECK inducers and determine their potential in blunting HF development and progression.