| Literature DB >> 33869659 |
C Ricordi1, L Inverardi1, A Pileggi1, R L Pastori1, J Dominguez-Bendala1.
Abstract
Diabetes is now considered a growing global epidemic with sizable negative effects on patients' quality of life and life expectancy, and escalating economic impact (41% growth in the past five year), now representing health care ex-penditure impact of 256 Billion/year in the US alone. Objectives of cellular therapies and regenerative medicine strategies for treatment of diabetes are to reverse the disease condition and prevent the development of the severe chronic complications that can affect most organ systems in a large proportion of patients over time. Cell based therapies include the combination of immunomodulatory approaches aimed at restoring self tolerance (i.e., in the case of autoimmune diabetes) and at inducing permanent acceptance of transplanted tissues (in the case of allogeneic donors), or immune protection (i.e., engineered microenvironment and/or encapsulation) so that the immune system can no longer destroy the new insulin producing cells introduced either by regenerating, reprogramming or replacement. Several approaches are currently under evaluation for restoration of beta cell mass. The prototype strategy for Replacement is pancreatic islet transplantation, which is now an approved procedure in several countries. Reprogramming from non insulin-producing cells or Regeneration strategies could represent an appealing alternative to overcome shortage of deceased donor organs for transplantation. The selection of the most appropriate source for insulin producing cells is still not defined and the selected alternatives between replacement, reprogramming and regeneration strategies will be further developed in pre-clinical model systems and pilot clinical trials, while carefully assessing safety, efficacy and cost-effectiveness, as well as the challenges imposed by scaling up the selected technologies to meet the demand of the millions of affected patients who could benefit from these strategies.Entities:
Year: 2014 PMID: 33869659 PMCID: PMC8048034
Source DB: PubMed Journal: CellR4 Repair Replace Regen Reprogram