Pancreatic beta-cells, which are the only cell type that produces and secretes insulin, play a crucial role in glucose homeostasis. The loss of beta-cell function or mass is a key feature of type 2 diabetes. Large-scale beta-cell dedifferentiation, characterized by a significant reduction in beta cell identity genes, suggests a dysfunctional and progenitor-like state. This immature state of beta-cells leads to impaired nutrient-stimulated insulin secretion and contributes to the onset of type 2 diabetes.
However, the exact mechanisms underlying beta-cell dedifferentiation require further investigation. Understanding the pathways that govern and regulate this process is essential for the development of therapies aimed at reversing the loss of identity and/or regenerating functional beta-cells for the treatment of diabetes.
We invite submissions for a special issue focusing on various aspects of beta-cell dedifferentiation, including, but not limited to:
• Molecular mechanisms underlying beta-cell dedifferentiation
• Cellular and molecular pathways involved in beta-cell reprogramming
• Cellular plasticity and regeneration of beta-cells
• The impact of environmental and genetic factors on beta-cell dedifferentiation
• Prevention or reversal of beta-cell dedifferentiation
We welcome original research articles, reviews, and mini-reviews for this special issue. All manuscripts should adhere to the guidelines and standards set by Frontiers in Endocrinology. Each submission will undergo a rigorous peer-review process conducted by experts in the field. We look forward to receiving your contributions to this important area of research.
Pancreatic beta-cells, which are the only cell type that produces and secretes insulin, play a crucial role in glucose homeostasis. The loss of beta-cell function or mass is a key feature of type 2 diabetes. Large-scale beta-cell dedifferentiation, characterized by a significant reduction in beta cell identity genes, suggests a dysfunctional and progenitor-like state. This immature state of beta-cells leads to impaired nutrient-stimulated insulin secretion and contributes to the onset of type 2 diabetes.
However, the exact mechanisms underlying beta-cell dedifferentiation require further investigation. Understanding the pathways that govern and regulate this process is essential for the development of therapies aimed at reversing the loss of identity and/or regenerating functional beta-cells for the treatment of diabetes.
We invite submissions for a special issue focusing on various aspects of beta-cell dedifferentiation, including, but not limited to:
• Molecular mechanisms underlying beta-cell dedifferentiation
• Cellular and molecular pathways involved in beta-cell reprogramming
• Cellular plasticity and regeneration of beta-cells
• The impact of environmental and genetic factors on beta-cell dedifferentiation
• Prevention or reversal of beta-cell dedifferentiation
We welcome original research articles, reviews, and mini-reviews for this special issue. All manuscripts should adhere to the guidelines and standards set by Frontiers in Endocrinology. Each submission will undergo a rigorous peer-review process conducted by experts in the field. We look forward to receiving your contributions to this important area of research.
