Matches in SemOpenAlex for { <https://semopenalex.org/work/W2230137209> ?p ?o ?g. }
- W2230137209 endingPage "162" @default.
- W2230137209 startingPage "153" @default.
- W2230137209 abstract "Stem cell therapies are finally coming of age in the context of pancreatic endocrine regeneration for diabetes. Clinical trials aimed at testing the safety and efficacy of human embryonic stem cell-derived islet surrogates are already ongoing. If successful, these approaches are expected to lead to the phasing out of the use of cadaveric islets for transplantation, exponentially extending our ability to treat millions of type 1 diabetes – and potentially also type 2 diabetes – patients. Different cell populations within the pancreas can regenerate the endocrine compartment through reprogramming, replication, or stimulation of resident progenitors. The field has recently advanced to the point where these phenomena can be induced without the need for genetic manipulation, getting us closer to the design of viable clinical trials for β cell replenishment or endogenous regeneration. Islet transplantation is an effective cell therapy for type 1 diabetes (T1D) but its clinical application is limited due to shortage of donors. After a decade-long period of exploration of potential alternative cell sources, the field has only recently zeroed in on two of them as the most likely to replace islets. These are pluripotent stem cells (PSCs) (through directed differentiation) and pancreatic non-endocrine cells (through directed differentiation or reprogramming). Here we review progress in both areas, including the initiation of Phase I/II clinical trials using human embryonic stem cell (hESc)-derived progenitors, advances in hESc differentiation in vitro, novel insights on the developmental plasticity of the pancreas, and groundbreaking new approaches to induce β cell conversion from the non-endocrine compartment without genetic manipulation. Islet transplantation is an effective cell therapy for type 1 diabetes (T1D) but its clinical application is limited due to shortage of donors. After a decade-long period of exploration of potential alternative cell sources, the field has only recently zeroed in on two of them as the most likely to replace islets. These are pluripotent stem cells (PSCs) (through directed differentiation) and pancreatic non-endocrine cells (through directed differentiation or reprogramming). Here we review progress in both areas, including the initiation of Phase I/II clinical trials using human embryonic stem cell (hESc)-derived progenitors, advances in hESc differentiation in vitro, novel insights on the developmental plasticity of the pancreas, and groundbreaking new approaches to induce β cell conversion from the non-endocrine compartment without genetic manipulation. islet cells that secrete insulin into the bloodstream in a glucose-responsive manner. They are primary targets in autoimmune T1D. β cell demise results in pathological hyperglycemia and lifelong need for exogenous insulin administration. In T2D, peripheral insulin resistance often leads to β cell exhaustion and death. As exogenous insulin is also required in severe T2D cases, strategies for β cell replenishment/regeneration are also potentially applicable. also known as the non-endocrine pancreatic compartment; comprises >95% of the organ, with the secretion of digestive enzymes as its primary function. This tissue comprises acinar and ductal cells. Acini are connected to the ductal system by centroacinar cells. The ductal tree drains digestive secretions to the duodenum through ducts of increasing caliber. the archetypical PSCs, obtained from the inner cell mass (ICM) of a human preimplantation embryo (d5–6 blastocyst). These cells are widely considered the gold standard of pluripotency. Embryonic germ (EG) cells are another example of native PSCs. new PSC types that do not exist in nature, derived by reprogramming differentiated cells. iPScs can theoretically be obtained from any individual. To most practical effects, iPScs and hEScs are functionally equivalent. also known as the endocrine pancreas, the islets of Langerhans are micro-organ-like cell clusters interspersed within the exocrine pancreas. They maintain glucose homeostasis by secreting specific hormones into the bloodstream. The main islet cell types are α (glucagon secreting), β (insulin secreting), δ (somatostatin secreting), PP (pancreatic polypeptide secreting), and ɛ (ghrelin secreting). a medical procedure by which islets from a cadaveric pancreas are separated from the non-endocrine fraction and then transplanted. Enzymatic digestion of the organ is followed by gradient separation of the various pancreatic fractions. Isolated islets are implanted in the liver through portal vein catheterization, although current clinical trials are exploring alternative placements such as the omentum (a visceral, highly vascularized fold of the peritoneum). Islet transplantation remains the standard cell therapy for T1D but is limited by the shortage of organs and the necessity for lifelong immunosuppression. cells with the ability to proliferate indefinitely in vitro under the right conditions while maintaining pluripotency; that is, the capacity to differentiate along all lineages of the three embryonic layers (endoderm, ectoderm, and mesoderm). non-terminally differentiated cells characterized by a variable degree of potency. Putative progenitor cells within the adult pancreas (PPcs) may be oligopotent (e.g., they would give rise to endocrine cells only) or multipotent (e.g., with multilineage differentiation potential spanning endocrine/exocrine fates). also called transdifferentiation; refers to a switch in cellular fate that is not brought about by differentiation. It typically refers to experimental methods (chiefly genetic/epigenetic manipulation) inducing the conversion of one cell type into another." @default.
- W2230137209 created "2016-06-24" @default.
- W2230137209 creator A5008060564 @default.
- W2230137209 creator A5037550785 @default.
- W2230137209 creator A5061358205 @default.
- W2230137209 creator A5067227229 @default.
- W2230137209 creator A5079442325 @default.
- W2230137209 date "2016-03-01" @default.
- W2230137209 modified "2023-10-05" @default.
- W2230137209 title "The Human Endocrine Pancreas: New Insights on Replacement and Regeneration" @default.
- W2230137209 cites W1655026638 @default.
- W2230137209 cites W1891286077 @default.
- W2230137209 cites W1950749075 @default.
- W2230137209 cites W1965974297 @default.
- W2230137209 cites W1967081779 @default.
- W2230137209 cites W1973453325 @default.
- W2230137209 cites W1973752547 @default.
- W2230137209 cites W1976829109 @default.
- W2230137209 cites W1977087101 @default.
- W2230137209 cites W1979001502 @default.
- W2230137209 cites W1981537118 @default.
- W2230137209 cites W1982098366 @default.
- W2230137209 cites W1992429625 @default.
- W2230137209 cites W1997670777 @default.
- W2230137209 cites W1999179141 @default.
- W2230137209 cites W2003454094 @default.
- W2230137209 cites W2005845399 @default.
- W2230137209 cites W2008360373 @default.
- W2230137209 cites W2011074645 @default.
- W2230137209 cites W2011702432 @default.
- W2230137209 cites W2015528355 @default.
- W2230137209 cites W2020496264 @default.
- W2230137209 cites W2022904783 @default.
- W2230137209 cites W2024090459 @default.
- W2230137209 cites W2025784989 @default.
- W2230137209 cites W2026925157 @default.
- W2230137209 cites W2026937301 @default.
- W2230137209 cites W2031611328 @default.
- W2230137209 cites W2032472678 @default.
- W2230137209 cites W2041739600 @default.
- W2230137209 cites W2048183701 @default.
- W2230137209 cites W2049820630 @default.
- W2230137209 cites W2052721366 @default.
- W2230137209 cites W2054361177 @default.
- W2230137209 cites W2057190776 @default.
- W2230137209 cites W2062960628 @default.
- W2230137209 cites W2064250803 @default.
- W2230137209 cites W2069863598 @default.
- W2230137209 cites W2075712485 @default.
- W2230137209 cites W2088927115 @default.
- W2230137209 cites W2089174697 @default.
- W2230137209 cites W2106219965 @default.
- W2230137209 cites W2107471483 @default.
- W2230137209 cites W2110509725 @default.
- W2230137209 cites W2114058685 @default.
- W2230137209 cites W2121134199 @default.
- W2230137209 cites W2125472394 @default.
- W2230137209 cites W2126780067 @default.
- W2230137209 cites W2132046208 @default.
- W2230137209 cites W2133186034 @default.
- W2230137209 cites W2137498184 @default.
- W2230137209 cites W2138726422 @default.
- W2230137209 cites W2140717092 @default.
- W2230137209 cites W2143406977 @default.
- W2230137209 cites W2143622229 @default.
- W2230137209 cites W2148147368 @default.
- W2230137209 cites W2148890861 @default.
- W2230137209 cites W2154532011 @default.
- W2230137209 cites W2157699156 @default.
- W2230137209 cites W2166089348 @default.
- W2230137209 cites W2168190340 @default.
- W2230137209 cites W2169191544 @default.
- W2230137209 cites W2169337437 @default.
- W2230137209 cites W2323566388 @default.
- W2230137209 cites W2328786770 @default.
- W2230137209 cites W4234853498 @default.
- W2230137209 cites W2079478904 @default.
- W2230137209 doi "https://doi.org/10.1016/j.tem.2015.12.003" @default.
- W2230137209 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26774512" @default.
- W2230137209 hasPublicationYear "2016" @default.
- W2230137209 type Work @default.
- W2230137209 sameAs 2230137209 @default.
- W2230137209 citedByCount "23" @default.
- W2230137209 countsByYear W22301372092016 @default.
- W2230137209 countsByYear W22301372092017 @default.
- W2230137209 countsByYear W22301372092018 @default.
- W2230137209 countsByYear W22301372092019 @default.
- W2230137209 countsByYear W22301372092020 @default.
- W2230137209 countsByYear W22301372092021 @default.
- W2230137209 countsByYear W22301372092022 @default.
- W2230137209 countsByYear W22301372092023 @default.
- W2230137209 crossrefType "journal-article" @default.
- W2230137209 hasAuthorship W2230137209A5008060564 @default.
- W2230137209 hasAuthorship W2230137209A5037550785 @default.
- W2230137209 hasAuthorship W2230137209A5061358205 @default.
- W2230137209 hasAuthorship W2230137209A5067227229 @default.
- W2230137209 hasAuthorship W2230137209A5079442325 @default.
- W2230137209 hasConcept C104317684 @default.