Diabetes is characterized by the inability to regulate blood glucose levels. Early in the disease process, our research focuses on regenerating the native pancreas, protecting islets and modulating the immune system through the local delivery of MSCs and MSC-EVs, while later in the disease process, our research focuses on optimizing islet transplantation which can replenish insulin-producing beta-cells.
Type 1 diabetes (T1D) is a chronic autoimmune disease caused by the selective destruction of insulin-producing β cells within pancreatic islets. Currently, T1D affects 1.4 million people in the United States and 30 million people globally, and its incidence is increasing at an alarming.
Recent studies have shown that diabetic patients still have residual β cells within their pancreas, which secrete low levels of insulin years after initial diagnosis. Hence, therapeutic interventions, like MSC-based therapies, hold great promise in recovering and/or regenerating residual β cell quantity and function, especially as they can modulate components of the immune system, inflammatory responses, stimulate neo-angiogenesis as well as protect islets from apoptosis and necrosis. Unfortunately, the clinical translation of MSC-based therapies for the treatment of diabetes has been sub-optimal due to their inability to reach the pancreas since parent MSCs get predominantly trapped in the lungs and EVs get trapped in organs of the reticuloendothelial system (RES) following conventional intravenous (IV) injection. Hence, in small animal models, we have developed a technique to deliver
deliver therapeutics, like MSCs, directly to the pancreas via its arterial blood supply given that this delivery can be easily accomplished in humans using endovascular techniques with the developments in new catheters (i.e. low-profile microcatheters) and imaging equipment (i.e. 3D fluoroscopic imaging).