About this Research Topic
Diabetes has truly reached worldwide epidemic proportions with 422 million sufferers identified in 2014 (WHO fact sheet). While diabetes can be managed, for many people the onset of life-threatening complications including blindness, kidney failure, heart attacks, stroke, and lower limb amputation further exacerbates the impact on mortality and morbidity. Today, identifying the mechanisms governing the onset and progression of complex conditions like diabetes still is exceedingly challenging, due to their multifactorial environmental component and the intricate genetic-susceptibility interaction.
Diabetes mellitus represents a group of energy metabolism diseases defined by hyperglycemia triggered by the inability of the body to produce and/or use sufficient insulin, where the two most common forms of the disease (Type 1 and Type 2 Diabetes) have a complex (polygenic and multifactorial) etiology. A key feature of many diabetic disorders is the loss of functional β-cells, whether by a loss of capability to release appropriate amounts of insulin in response to changing glucose levels or by physical cellular loss. It remains largely unknown what the external factors are, what cellular signals are leading to insulin-producing β-cell decay, and what cellular processes and molecular mechanisms characterize this transition. In addition, the role of the other pancreatic cell populations in diabetes is just now starting to emerge.
The realization that beta-cell dysfunction is one key element leading to diabetes, has led to the development of strategies to replace beta-cells. Initiated with transplantation of the whole pancreas and adult islets both from cadaveric organ donors, the field is on the verge of clinical testing of alternate beta-cell sources including stem cell-derived cellular products and islets harvested from xenogeneic sources. Long-term studies suggest beta-cell failure after transplantation may replicate the initial disease-causing mechanisms leading to endogenous beta-cell failure. Thus, our lack of knowledge regarding primary disease mechanism may hinder the progress of replacement strategies.
Genome-wide association studies and classical linkage analysis has revealed the genetic heterogeneity of T1D and T2D. Many of the associated genes are expressed by beta-cells and yet the function of most identified genes in normal beta-cell function and how they may contribute to the beta cell dysfunction is still unknown. This Research Topic aims to provide a comprehensive picture of current studies focused on molecular circuits involved in insulin-producing beta cell’s development, function and dysfunction, touching multiple aspects of islet niche. Original Research, Methods, Review, Mini Review, Perspective, and Opinion articles addressing the following topics and other similar studies are welcome:
• Islet cell interactions and communication
• Islet cell interconversion
• Crosstalk with the islet microenvironment
• Genetic and/or epigenetic reprogramming
• Genome-wide association studies
• Functional genomics
• In vitro differentiation
• Targeted pathways modulations
Diabetes mellitus represents a group of energy metabolism diseases defined by hyperglycemia triggered by the inability of the body to produce and/or use sufficient insulin, where the two most common forms of the disease (Type 1 and Type 2 Diabetes) have a complex (polygenic and multifactorial) etiology. A key feature of many diabetic disorders is the loss of functional β-cells, whether by a loss of capability to release appropriate amounts of insulin in response to changing glucose levels or by physical cellular loss. It remains largely unknown what the external factors are, what cellular signals are leading to insulin-producing β-cell decay, and what cellular processes and molecular mechanisms characterize this transition. In addition, the role of the other pancreatic cell populations in diabetes is just now starting to emerge.
The realization that beta-cell dysfunction is one key element leading to diabetes, has led to the development of strategies to replace beta-cells. Initiated with transplantation of the whole pancreas and adult islets both from cadaveric organ donors, the field is on the verge of clinical testing of alternate beta-cell sources including stem cell-derived cellular products and islets harvested from xenogeneic sources. Long-term studies suggest beta-cell failure after transplantation may replicate the initial disease-causing mechanisms leading to endogenous beta-cell failure. Thus, our lack of knowledge regarding primary disease mechanism may hinder the progress of replacement strategies.
Genome-wide association studies and classical linkage analysis has revealed the genetic heterogeneity of T1D and T2D. Many of the associated genes are expressed by beta-cells and yet the function of most identified genes in normal beta-cell function and how they may contribute to the beta cell dysfunction is still unknown. This Research Topic aims to provide a comprehensive picture of current studies focused on molecular circuits involved in insulin-producing beta cell’s development, function and dysfunction, touching multiple aspects of islet niche. Original Research, Methods, Review, Mini Review, Perspective, and Opinion articles addressing the following topics and other similar studies are welcome:
• Islet cell interactions and communication
• Islet cell interconversion
• Crosstalk with the islet microenvironment
• Genetic and/or epigenetic reprogramming
• Genome-wide association studies
• Functional genomics
• In vitro differentiation
• Targeted pathways modulations
Keywords: Genetics of diabetes, Epigenetics, Pancreatic Islet Microenvironment, Beta cell replacement, Stem Cells
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