Pancreatic islets are specialized clusters of endocrine cells containing insulin-producing beta cells, glucagon-producing alpha cells, and somatostatin-producing delta cells, among others. Diabetes is a consequence of the inability to adequately secrete insulin, in combination or not, to decreased capacity to respond to this hormone. Type 1 diabetes results from autoimmune-dependent beta cell death, whilst Type 2 diabetes is frequently a consequence of obesity and poor health habits, also leading to beta-cell dysfunction and death. Moreover, beta-cells isolated from patients with Type 2 diabetes have been shown to have senescence markers, such as senescence-associated secretory phenotype genes and ß-galactosidase. Although Type 1- and Type 2 diabetes have different etiology, the molecular mechanisms involved in beta cell senescence and death can have similar mechanistic underpinnings, such as Endoplasmic Reticulum Stress, increased reactive oxygen species production, and the cytotoxic effects of cytokines, chemokines, lipids, and glucose.
While the mechanistic processes mediating beta-cell death in both Type 1 and Type 2 diabetes are quite well described, we have much less understanding of the hierarchy, cross-talk, and interplay of the various cell death mechanisms. Moreover, the role of other islet cell types in beta-cell dysfunction and death is not fully understood. Better knowledge of the ‘big picture’ of beta-cell senescence and death will help to advance therapeutic interventions, for example, the development of new drugs as well as other promising strategies, including islet transplantation.
We welcome different kinds of articles, including original research articles, reviews, mini-reviews, and opinion/perspectives, which cover, but not limited to, the following themes:
- how different pathways interconnect, communicate and influence each other in pancreatic islets in Type 1 and Type 2 diabetes;
- new information on the complex pancreatic setting, elucidating pathways hierarchy, interplays, and cross-talks;
- the molecular basis of different therapeutic strategies, in particular the effect of different drugs on the molecular pathways and the mechanisms of islet adaptation during transplantation.
Pancreatic islets are specialized clusters of endocrine cells containing insulin-producing beta cells, glucagon-producing alpha cells, and somatostatin-producing delta cells, among others. Diabetes is a consequence of the inability to adequately secrete insulin, in combination or not, to decreased capacity to respond to this hormone. Type 1 diabetes results from autoimmune-dependent beta cell death, whilst Type 2 diabetes is frequently a consequence of obesity and poor health habits, also leading to beta-cell dysfunction and death. Moreover, beta-cells isolated from patients with Type 2 diabetes have been shown to have senescence markers, such as senescence-associated secretory phenotype genes and ß-galactosidase. Although Type 1- and Type 2 diabetes have different etiology, the molecular mechanisms involved in beta cell senescence and death can have similar mechanistic underpinnings, such as Endoplasmic Reticulum Stress, increased reactive oxygen species production, and the cytotoxic effects of cytokines, chemokines, lipids, and glucose.
While the mechanistic processes mediating beta-cell death in both Type 1 and Type 2 diabetes are quite well described, we have much less understanding of the hierarchy, cross-talk, and interplay of the various cell death mechanisms. Moreover, the role of other islet cell types in beta-cell dysfunction and death is not fully understood. Better knowledge of the ‘big picture’ of beta-cell senescence and death will help to advance therapeutic interventions, for example, the development of new drugs as well as other promising strategies, including islet transplantation.
We welcome different kinds of articles, including original research articles, reviews, mini-reviews, and opinion/perspectives, which cover, but not limited to, the following themes:
- how different pathways interconnect, communicate and influence each other in pancreatic islets in Type 1 and Type 2 diabetes;
- new information on the complex pancreatic setting, elucidating pathways hierarchy, interplays, and cross-talks;
- the molecular basis of different therapeutic strategies, in particular the effect of different drugs on the molecular pathways and the mechanisms of islet adaptation during transplantation.
