Hardikar Anandwardhan A
National Institute of Diabetes and Digestive and Kidney Diseases, Bldg 50/Room 4128, National Institutes of Health, Bethesda, MD 20892, USA.
Trends Endocrinol Metab. 2004 Jul;15(5):198-203. doi: 10.1016/j.tem.2004.05.001.
Pancreas regeneration after tissue damage is a key response to pancreatic injury, involving pancreatic duct progenitor cells and intra-islet precursor cells. Surgical removal of the pancreas, duct obstruction by cellophane wrapping and bone marrow-derived stem cell transplantation act as inductive stimuli, leading to pancreas regeneration. The exact role of growth and differentiation factors regulating pancreatic beta-cell mass remains unknown. Here, I will attempt to integrate recent findings and speculate on the factors that trigger this fascinating response, wherein the pancreas responds to a deficit in cell mass and undergoes new islet formation, leading to restoration of normal beta-cell mass. I will also discuss recent advances in regenerating endocrine pancreatic cells, which could affect stem cell-based approaches to treating diabetes mellitus.
组织损伤后胰腺再生是胰腺损伤的关键反应,涉及胰腺导管祖细胞和胰岛内前体细胞。手术切除胰腺、用玻璃纸包裹造成导管阻塞以及骨髓来源的干细胞移植作为诱导刺激,可导致胰腺再生。调节胰腺β细胞量的生长和分化因子的确切作用尚不清楚。在此,我将尝试整合近期的研究发现,并推测引发这种迷人反应的因素,即胰腺对细胞量不足作出反应并经历新胰岛形成,从而恢复正常β细胞量。我还将讨论内分泌胰腺细胞再生方面的最新进展,这可能会影响基于干细胞的糖尿病治疗方法。