Peng Wang

TL;DR: Using three different mouse and human islet in vivo–based models, harmine is able to induce beta cell proliferation, increase islet mass and improve glycemic control, suggesting that harmine analogs may have unique therapeutic promise for human diabetes therapy.

TL;DR: The physiology of normal human β-cell replication, the molecular mechanisms that regulate the cell cycle in human β cells, the upstream intracellular signalling pathways that connect them to cell surface receptors on β cells and unbiased approaches for discovering novel molecules that can drive humanβ-cell proliferation are discussed.

TL;DR: Combined pharmacologic inhibition of DYRK1A and transforming growth factor beta superfamily (TGFβSF)/SMAD signaling generates remarkable further synergistic increases in human beta cell proliferation, and increases in both mouse and human beta cells numbers.

TL;DR: It is shown at the pathway level that the majority of the insulinomas display mutations, copy number variants and/or dysregulation of epigenetic modifying genes, most prominently in the polycomb and trithorax families, revealing candidates for inducing beta cell regeneration.

TL;DR: The ability of the GLP1R agonist–DYRK1A inhibitor combination to enhance human β cell proliferation, human insulin secretion, and blood glucose control extended in vivo to studies of human islets transplanted into euglycemic and streptozotocin-diabetic immunodeficient mice.