The loss of pancreatic beta cell mass and function has a major role in the pathogenesis of both type 1 diabetes (T1D) and type 2 diabetes (T2D). In this respect, major research efforts have been made on maintaining/increasing beta cell mass and on rescuing beta cell function. There is, however, still a long way to go to turn some of these efforts into new therapies to treat diabetic patients.
A large body of research in the area of diabetes is focused on developing strategies to induce beta cell proliferation. This is a major challenge because beta cells have a very low proliferation rate, especially in human adults. Furthermore, pathways driving proliferation are compromised in T2D.
Preserving beta cell mass by preventing beta cell death is also a major field of research in both T1D and T2D. Targeting beta cells in order to make them more resilient will not only protect them from cell death but will also contribute to the maintenance of beta cell function.
Even when there is no decrease in beta cell mass, impairment of beta cell function occurs in T2D leading to a decline in insulin production. In this context, during the last decades, the main therapeutic strategy to improve beta cell function was aimed at amplifying beta cell insulin secretion. However, this may not be a completely successful strategy, (e.g. sulfonylureas) since may lead to beta cell exhaustion and failure. As an alternative, therapeutic interventions aiming at protecting and preserving beta cell function without directly targeting insulin secretion might prove to be a more successful approach in the treatment of T2D. Maintaining the function of remaining beta cells in T1D has also been shown to have a major positive impact on the prognosis of the disease and the development of diabetic complications.
The goal of this research topic is to open new avenues with relevance for T1D and T2D treatment. These will include:
- identification of new pathways, genes, signaling molecules, and therapies that preserve/increase beta cell mass and/or function;
- new insights into known pathways, genes, signaling molecules, and therapies relevant for beta cell mass and/or function.
More in detail, this Research Topic will mainly focus on three main areas:
• Studies focusing on inducing beta cell proliferation, including mechanisms and strategies to induce beta cell division, cell-type specificity and phenotypic characterization of these cells;
• Research buckling down to beta cell function, comprising new pathways, genes, and signalling molecules critical for beta cell maturation and metabolism, as well as insights into cellular senescence in diabetes and senolysis strategies to treat diabetes;
• Investigation of beta cell survival, inclusive of targeting the production of inflammatory cytokines, suppression of cytokine-induced beta cell apoptosis and response to metabolic, ER and/or oxidative stress.
The loss of pancreatic beta cell mass and function has a major role in the pathogenesis of both type 1 diabetes (T1D) and type 2 diabetes (T2D). In this respect, major research efforts have been made on maintaining/increasing beta cell mass and on rescuing beta cell function. There is, however, still a long way to go to turn some of these efforts into new therapies to treat diabetic patients.
A large body of research in the area of diabetes is focused on developing strategies to induce beta cell proliferation. This is a major challenge because beta cells have a very low proliferation rate, especially in human adults. Furthermore, pathways driving proliferation are compromised in T2D.
Preserving beta cell mass by preventing beta cell death is also a major field of research in both T1D and T2D. Targeting beta cells in order to make them more resilient will not only protect them from cell death but will also contribute to the maintenance of beta cell function.
Even when there is no decrease in beta cell mass, impairment of beta cell function occurs in T2D leading to a decline in insulin production. In this context, during the last decades, the main therapeutic strategy to improve beta cell function was aimed at amplifying beta cell insulin secretion. However, this may not be a completely successful strategy, (e.g. sulfonylureas) since may lead to beta cell exhaustion and failure. As an alternative, therapeutic interventions aiming at protecting and preserving beta cell function without directly targeting insulin secretion might prove to be a more successful approach in the treatment of T2D. Maintaining the function of remaining beta cells in T1D has also been shown to have a major positive impact on the prognosis of the disease and the development of diabetic complications.
The goal of this research topic is to open new avenues with relevance for T1D and T2D treatment. These will include:
- identification of new pathways, genes, signaling molecules, and therapies that preserve/increase beta cell mass and/or function;
- new insights into known pathways, genes, signaling molecules, and therapies relevant for beta cell mass and/or function.
More in detail, this Research Topic will mainly focus on three main areas:
• Studies focusing on inducing beta cell proliferation, including mechanisms and strategies to induce beta cell division, cell-type specificity and phenotypic characterization of these cells;
• Research buckling down to beta cell function, comprising new pathways, genes, and signalling molecules critical for beta cell maturation and metabolism, as well as insights into cellular senescence in diabetes and senolysis strategies to treat diabetes;
• Investigation of beta cell survival, inclusive of targeting the production of inflammatory cytokines, suppression of cytokine-induced beta cell apoptosis and response to metabolic, ER and/or oxidative stress.