Decoding and understanding molecular mechanisms: Cell signaling pathways, pancreatic β-cell regeneration, and stem cell niche engineering for diabetes

Abstract

Stem cell bioengineering addresses regenerative medicine and cellular therapies by applying advanced techniques to stem-cell-derived systems. Despite their promise, stem cell applications are limited by incomplete knowledge. Stem cells and phytochemicals show potential in treating diabetes by halting β-cell degeneration and promoting endogenous islet regeneration. Current diabetes cell therapies include stem cells, mature pancreatic cells, endocrine progenitors, and β-cells, with researchers actively seeking new cell sources for clinically relevant β-cells. Stem cell-derived pancreatic cells are particularly promising for pancreatic islet regeneration. Diabetes mellitus results from cell loss or malfunction: Type 1 diabetes stems from autoimmune damage, whereas Type 2 diabetes is largely attributed to cell malfunction or insulin resistance. The only operative therapy, islet transplantation, necessitates lifelong immune suppression. Significant progress has been made in strategies for therapeutic adult β-cell regeneration. This review assesses studies on cellular signaling pathways linked to β-cell survival and proliferation, exploring regenerative medicine methodologies for pancreatic islet replacement or regeneration. While the “replacement” technique involves cell transplantation, the “regeneration” strategy preserves cell populations through replication. Moreover, artemether and gamma-aminobutyric acid induce pancreatic cells to adopt β-cell-like phenotypes, potentially aiding in the development of new β-cell-like cells for treating severe diabetes in rats. Understanding G-protein-coupled receptor activation pathways is crucial, as new treatment strategies for insulin-dependent diabetic mellitus may emerge from this knowledge.