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Biomedicines
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Novel Insights into the Mechanisms Leading to β-Cell Dysfunction and...
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Novel Insights into the Mechanisms Leading to β-Cell Dysfunction and Demise in Type 1 Diabetes

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 4187

Special Issue Editors

Dr. Laura Marroqui

E-Mail Website
Guest Editor
Instituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE), Universidad Miguel Hernández de Elche, 03202 Elche, Spain
Interests: type 1 diabetes; interferon pathway; pancreatic islets
Dr. Reinaldo Sousa Dos Santos

E-Mail Website
Guest Editor
​Instituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche, ​Universidad Miguel Hernández de Elche, Elche, Spain
Interests: diabetes; pancreatic beta cells; type 1 diabetes

Special Issue Information

Dear Colleagues,

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by pancreatic islet inflammation (insulitis) and specific pancreatic β-cell destruction by the immune system. Although the precise etiology and pathological mechanisms leading to the autoimmune attack are mostly unclear, it is well accepted that insulitis takes place in the context of a conflicting dialogue between the immune cells, which release cytokines and chemokines into the islet microenvironment and deliver pro-apoptotic signals, and pancreatic β-cells, which generates signals that will attract and activate immune cells to the islets. This dialogue is determined by multiple combinations of the host genetic susceptibility (i.e., candidate genes) and environmental factors (e.g., viral infections and diet).

In this Special Issue, we are interested in studies that further contribute to the mechanisms and signaling pathways underlying β-cell dysfunction and death in the context of type 1 diabetes. Additionally, we welcome manuscripts that provide insights into mechanisms of β-cell protection against inflammation and immune attack.

We accept contributions to, but not limited to, the following themes:

  • Genetic and environmental factors leading to β-cell dysfunction and apoptosis;
  • Signaling pathways altered in β-cells under a proinflammatory context;
  • Metabolic and functional changes in β-cells under a proinflammatory context;
  • Mechanisms of β-cell survival against proinflammatory cytokines;
  • Possible targets for β-cell protection that could lead to the prevention and treatment of type 1 diabetes.

Dr. Laura Marroqui
Dr. Reinaldo Sousa Dos Santos
Guest Editors

Keywords

  • type 1 diabetes
  • pancreatic beta cells
  • insulitis
  • cytokines
  • T1D prevention and treatment

Published Papers (2 papers)

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Research

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8 pages, 663 KiB  
Communication
Role of HNFA1 Gene Variants in Pancreatic Beta Cells Function and Glycaemic Control in Young Individuals with Type 1 Diabetes
by Antonietta Robino, Gianluca Tornese, Davide Tinti, Klemen Dovc, Valeria Castorani, Andrea Conti, Roberto Franceschi, Ivana Rabbone, Riccardo Bonfanti, Tadej Battelino and Eulalia Catamo
Biomedicines 2023, 11(7), 1951; https://doi.org/10.3390/biomedicines11071951 - 10 Jul 2023
Viewed by 1115
Abstract
The HNF1A transcription factor, implicated in the regulation of pancreatic beta cells, as well as in glucose and lipid metabolism, is responsible for type 3 maturity-onset diabetes of the young (MODY3). HNF1A is also involved in increased susceptibility to polygenic forms of diabetes, [...] Read more.
The HNF1A transcription factor, implicated in the regulation of pancreatic beta cells, as well as in glucose and lipid metabolism, is responsible for type 3 maturity-onset diabetes of the young (MODY3). HNF1A is also involved in increased susceptibility to polygenic forms of diabetes, such as type 2 diabetes (T2D) and gestational diabetes (GD), while its possible role in type 1 diabetes (T1D) is not known. In this study, 277 children and adolescents with T1D and 140 healthy controls were recruited. The following SNPs in HNF1A gene were selected: rs1169286, rs1169288, rs7979478, and rs2259816. Through linear or logistic regression analysis, we analyzed their association with T1D susceptibility and related clinical traits, such as insulin dose-adjusted glycated hemoglobin A1c (IDAA1c) and glycated hemoglobin (HbA1c). We found that rs1169286 was associated with IDAA1c and HbA1c values (p-value = 0.0027 and p-value = 0.0075, respectively), while rs1169288 was associated with IDAA1c (p-value = 0.0081). No association between HNF1A SNPs and T1D development emerged. In conclusion, our findings suggest for the first time that HNF1A variants may be a risk factor for beta cell function and glycaemic control in T1D individuals. Full article
(This article belongs to the Special Issue Novel Insights into the Mechanisms Leading to β-Cell Dysfunction and Demise in Type 1 Diabetes)
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Review

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12 pages, 1441 KiB  
Review
Revisiting the Pathogenesis of Type 1 Diabetes: Importance of Neural Input to Pancreatic Islets and the Therapeutic Capability of Stem Cell Educator TM Therapy to Restore Their Integrity
by Yong Zhao and Boris Veysman
Biomedicines 2023, 11(2), 594; https://doi.org/10.3390/biomedicines11020594 - 16 Feb 2023
Cited by 2 | Viewed by 2304
Abstract
Type 1 diabetes (T1D) is an autoimmune disease with a shortage of islet β cells. To date, the etiology of T1D remains elusive. Increasing clinical evidence and animal studies demonstrate that autoimmune cells are directed against the nervous system of pancreatic islets, contributing [...] Read more.
Type 1 diabetes (T1D) is an autoimmune disease with a shortage of islet β cells. To date, the etiology of T1D remains elusive. Increasing clinical evidence and animal studies demonstrate that autoimmune cells are directed against the nervous system of pancreatic islets, contributing to the development of T1D. Therefore, it highlights the necessity to explore novel clinical approaches to fundamentally correct the T1D autoimmunity not only focusing on islet β cells but also on protecting the islet nervous system. This allows the restoration of the integrity of islet innervation and the normal islet β-cell function. To address these issues, we developed a novel technology designated the Stem Cell Educator TM therapy, based on immune education by human cord-blood-derived multipotent stem cells (CB-SC). International amulticenter clinical trials demonstrated its clinical safety and efficacy to treat T1D and other autoimmune diseases. Stem Cell Educator TM therapy may have the potential to revolutionize the treatment of T1D, without the safety and ethical concerns associated with conventional immune and/or stem cell-based therapies. Full article
(This article belongs to the Special Issue Novel Insights into the Mechanisms Leading to β-Cell Dysfunction and Demise in Type 1 Diabetes)
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