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Molecular Research on Type 1 Diabetes and Its Complications: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 549

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Guest Editor
Clinical Physiology Unit, Medical Simulation Centre, Medical University of Gdańsk, Gdansk, Poland
Interests: endothelial dysfunction; microcirculation; macrocirculation; diabetes mellitus; cardiovascular diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue, “Molecular Research on Type 1 Diabetes and Its Complications”. The prevalence of type 1 diabetes is steadily increasing, especially in developed countries. Despite significant improvements in the diagnosis, prevention and treatment of diabetes complications based on interdisciplinary diabetes care, its chronic complications in the form of microangiopathies and macroangiopathies are a major cause of disability and reduced quality of life. In addition, mortality in type 1 diabetes remains two to eight times higher than in the general population. The main causes of mortality are cardiovascular complications, including cardiovascular and cerebrovascular events. The pathophysiological and morphological basis for the development of diabetic complications remains unclear. Endothelial damage during hyperglycemia and persistent inflammation in the microcirculation are responsible for microangiopathies such as retinopathy, neuropathy, nephropathy or cutaneous angiopathy. Another factor that increases inflammation in type 1 diabetes is the autoimmune nature of the disease. Many studies are devoted to investigating the impact of gene polymorphisms on the development of diabetic complications and searching for potential treatments. Personalization of preventive and therapeutic interventions is important. Undoubtedly, the future of type 1 diabetes treatment is linked to regenerative medicine.

This Special Issue of the International Journal of Molecular Sciences focuses on the latest research on the pathogenesis, early diagnosis or treatment of type 1 diabetes and its complications with both conventional and innovative technologies. This Special Issue welcomes in vitro and in vivo studies, as well as original research and reviews.

Dr. Jolanta Neubauer-Geryk
Guest Editor

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Keywords

  • type 1 diabetes mellitus
  • diabetic microangiopathy
  • diabetic macroangiopathy
  • continuous glucose monitoring
  • experimental diabetic models
  • biomarkers
  • endothelium dysfunction
  • diabetes-related diseases
  • comorbidities
  • pregnancy
  • pathophysiology
  • metabolic syndrome
  • treatment
  • precision medicine

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Published Papers (1 paper)

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13 pages, 3997 KiB  
Article
Transient Inflammation of Pancreatic Exocrine Tissue in Autoimmune Diabetes Follows Onset of Islet Damage and Utilizes Heparanase-1
by Charmaine J. Simeonovic, Zuopeng Wu, Sarah K. Popp, Gerard F. Hoyne and Christopher R. Parish
Int. J. Mol. Sci. 2025, 26(9), 4120; https://doi.org/10.3390/ijms26094120 - 26 Apr 2025
Viewed by 197
Abstract
Inflammation of the exocrine pancreas accompanies autoimmune diabetes in mouse models and humans. However, the relationship between inflammation in the exocrine and endocrine (islet) compartments has not been explored. To address this issue, we used a transgenic mouse model in which autoimmune diabetes [...] Read more.
Inflammation of the exocrine pancreas accompanies autoimmune diabetes in mouse models and humans. However, the relationship between inflammation in the exocrine and endocrine (islet) compartments has not been explored. To address this issue, we used a transgenic mouse model in which autoimmune diabetes is acutely induced after the transfer of islet beta cell-specific transgenic T cells. Histological analyses demonstrated that inflammation of the exocrine pancreas, which was initially mild, resulted in the transient but widespread disruption of acinar tissue. Islet inflammation preceded exacerbated exocrine pathology, progressed to T cell-induced islet damage/destruction and persisted when exocrine inflammation subsided. Heparanase-1 (HPSE-1), an endoglycosidase that degrades heparan sulfate in basement membranes (BMs), when preferentially expressed in recipient cells but not donor (HPSE-1-deficient (HPSE-KO)) T cells, played a critical role in both exocrine and islet inflammation. In this context, HPSE-1 facilitates the passage of autoimmune T cells across the sub-endothelial basement membrane (BM) of pancreatic blood vessels and initially into the exocrine tissue. Peak exocrine inflammation that preceded or accompanied the acute onset of diabetes and HPSE-1 potentially contributed to acinar damage. In contrast to inflammation, HPSE-1 expressed by donor T cells played a key role in the induction of diabetes by allowing autoimmune T cells to traverse peri-islet BMs in order to destroy insulin-producing beta cells. Overall, our findings suggest that major exocrine pancreas injury is not required for the initiation of autoimmune islet damage and is not essential at the time of diabetes onset. Full article
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