RT Journal Article
T1 Harnessing the Endogenous Plasticity of Pancreatic Islets: A Feasible Regenerative Medicine Therapy for Diabetes?
A1 Lorenzo, Petra I
A1 Cobo-Vuilleumier, Nadia
A1 Martín-Vázquez, Eugenia
A1 López-Noriega, Livia
A1 Gauthier, Benoit R
K1 HMG20A
K1 LRH-1/NR52A
K1 PAX4
K1 diabetes
K1 redifferentiation
K1 regeneration
K1 single-cell transcriptomics
K1 transdifferentiation
K1 β-cell heterogeneity
AB Diabetes is a chronic metabolic disease caused by an absolute or relative deficiency in functional pancreatic β-cells that leads to defective control of blood glucose. Current treatments for diabetes, despite their great beneficial effects on clinical symptoms, are not curative treatments, leading to a chronic dependence on insulin throughout life that does not prevent the secondary complications associated with diabetes. The overwhelming increase in DM incidence has led to a search for novel antidiabetic therapies aiming at the regeneration of the lost functional β-cells to allow the re-establishment of the endogenous glucose homeostasis. Here we review several aspects that must be considered for the development of novel and successful regenerative therapies for diabetes: first, the need to maintain the heterogeneity of islet β-cells with several subpopulations of β-cells characterized by different transcriptomic profiles correlating with differences in functionality and in resistance/behavior under stress conditions; second, the existence of an intrinsic islet plasticity that allows stimulus-mediated transcriptome alterations that trigger the transdifferentiation of islet non-β-cells into β-cells; and finally, the possibility of using agents that promote a fully functional/mature β-cell phenotype to reduce and reverse the process of dedifferentiation of β-cells during diabetes.
YR 2021
FD 2021-04-19
LK http://hdl.handle.net/10668/17697
UL http://hdl.handle.net/10668/17697
LA en
DS RISalud
RD May 11, 2025