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

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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 February 2026 | Viewed by 3875

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Dr. Jolanta Neubauer-Geryk

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Clinical Physiology Unit, Medical Simulation Centre, Medical University of Gdańsk, Gdansk, Poland
Interests: endothelial dysfunction; microcirculation; macrocirculation; diabetes mellitus; cardiovascular diseases
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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 (5 papers)

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Research

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17 pages, 1756 KB

Open AccessArticle

Parameters of Micro- and Macrocirculation in Young Uncomplicated Type 1 Diabetic Patients—The Role of Metabolic Memory

by Jolanta Neubauer-Geryk, Małgorzata Myśliwiec, Katarzyna Zorena and Leszek Bieniaszewski

Int. J. Mol. Sci. 2025, 26(20), 10156; https://doi.org/10.3390/ijms262010156 - 18 Oct 2025

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Abstract

In the current study, we focus on analyzing the relationship between changes in micro- and macrocirculation and different stages of metabolic memory. We hypothesized that early poor glycemic control induces lasting endothelial changes detectable in pediatric type 1 diabetes (T1D) microcirculation. We assessed microcirculation structure and function using capillaroscopy, transcutaneous oxygen pressure (TcPO₂), and optical coherence tomography (OCT). We evaluated macrovascular circulation using pulsatility index (PI), ankle-brachial index (ABI) and pulse pressure (PP). We also examined the relationship between circulation parameters, the age at onset, and diabetes duration. The study included 67 patients with uncomplicated type 1. We divided all patients into four groups based on their HbA_1c levels at T1D onset and their average HbA_1c after one and two years. We assessed the concentrations of TNF-α, IL-35, IL-4, IL-10, IL-18, IL-12, serum angiogenin, VEGF, sVCAM-1, ICAM-1, sP-Selectin, AGEs, and sRAGE. We compared subgroups with different levels of metabolic memory but comparable T1D duration and age at diagnosis. Micro- and macrovascular parameters were similar between the groups. Our comparison of subgroups with identical metabolic memory but different durations and ages at diagnosis revealed clear differences. The subgroup with a shorter T1D duration showed higher capillary density and a smaller inter-capillary distance compared to those with a longer diabetes duration. This subgroup with shorter duration had significantly lower AGE levels and a reduced TNF-α/IL-35 ratio, along with higher levels of IL-35, IL-4, and IL-12, compared to the longer-duration group. Our findings indicate that in youths with uncomplicated T1D, disease duration—not metabolic memory—plays a dominant role in early microvascular alterations. Full article

(This article belongs to the Special Issue Molecular Research on Type 1 Diabetes and Its Complications: 2nd Edition)

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18 pages, 3248 KB

Open AccessArticle

Electrochemical Nanostructured Aptasensor for Direct Detection of Glycated Hemoglobin

by Luminita Fritea, Cosmin-Mihai Cotrut, Iulian Antoniac, Simona Daniela Cavalu, Luciana Dobjanschi, Angela Antonescu, Liviu Moldovan, Maria Domuta and Florin Banica

Int. J. Mol. Sci. 2025, 26(15), 7140; https://doi.org/10.3390/ijms26157140 - 24 Jul 2025

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Abstract

Glycated hemoglobin (HbA1c) is an important biomarker applied for the diagnosis, evaluation, and management of diabetes; therefore, its accurate determination is crucial. In this study, an innovative nanoplatform was developed, integrating carbon nanotubes (CNTs) with enhanced hydrophilicity achieved through cyclodextrin (CD) functionalization, and combined with gold nanoparticles (AuNPs) electrochemically deposited onto a screen-printed carbon electrode. The nanomaterials significantly improved the analytical performance of the sensor due to their increased surface area and high electrical conductivity. This nanoplatform was employed as a substrate for the covalent attachment of thiolated ferrocene-labeled HbA1c specific aptamer through Au-S binding. The electrochemical signal of ferrocene was covered by a stronger oxidation peak of Fe²⁺ from the HbA1c structure, leading to the elaboration of a nanostructured aptasensor capable of the direct detection of HbA1c. The electrochemical aptasensor presented a very wide linear range (0.688–11.5%), an acceptable limit of detection (0.098%), and good selectivity and stability, being successfully applied on real samples. This miniaturized, simple, easy-to-use, and fast-responding aptasensor, requiring only a small sample volume, can be considered as a promising candidate for the efficient on-site determination of HbA1c. Full article

(This article belongs to the Special Issue Molecular Research on Type 1 Diabetes and Its Complications: 2nd Edition)

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12 pages, 796 KB

Open AccessArticle

Maternal Vascular Adaptation in High-Risk Pregnancies: Effects of Early Smoking Cessation on Hemodynamic and Endothelial Function

by Kaltrina Kutllovci Hasani, Mila Cervar-Zivkovic, Ursula Hiden, Adam Saloň, Manurishi Nanda, Bianca Steuber, Katharina Eberhard, Patrick De Boever, Christina Stern, Karoline Mayer-Pickel and Nandu Goswami

Int. J. Mol. Sci. 2025, 26(12), 5781; https://doi.org/10.3390/ijms26125781 - 16 Jun 2025

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Abstract

Cardiovascular adaptation is vital for a healthy pregnancy but may be impaired in women at high risk for preeclampsia (PE), a condition marked by endothelial dysfunction. Smoking may lower the PE risk but harms vessels, and the effects of early cessation remain unclear. This prospective cohort study assessed vascular changes in high-risk pregnancies and the potential influence of early smoking cessation. Of 110 women screened for PE in the first trimester, 43 were classified as high-risk: 18 former smokers and 25 lifelong non-smokers. Vascular assessments were performed at 11–16, 24–28, and 34–37 weeks of gestation. Parameters included the carotid–femoral pulse wave velocity (cfPWV), asymmetric dimethylarginine (ADMA), mean arterial pressure (MAP), systolic and diastolic blood pressure (SBP, DBP), heart rate (HR), and retinal vessel calibers (central retinal arteriolar and venular equivalents (CRAE, CRVE)). Serum cotinine confirmed abstinence in former smokers. Across gestation, ADMA (p = 0.034), MAP (p = 0.001), SBP (p = 0.033), DBP (p = 0.004), and HR (p = 0.004) increased, while CRAE (p = 0.016) and CRVE (p = 0.004) narrowed in late pregnancy; cfPWV remained stable (p = 0.783). Non-smokers showed increases in their ADMA (p = 0.020), MAP (p = 0.001), and DBP (p = 0.0001) with no differences between groups. High-risk pregnancies showed vascular changes with similar profiles in former and non-smokers, underscoring the need for broader studies. Full article

(This article belongs to the Special Issue Molecular Research on Type 1 Diabetes and Its Complications: 2nd Edition)

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13 pages, 3997 KB

Open AccessArticle

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

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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 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

(This article belongs to the Special Issue Molecular Research on Type 1 Diabetes and Its Complications: 2nd Edition)

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Review

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26 pages, 735 KB

Open AccessReview

Protective Effects of PACAP in Diabetic Complications: Retinopathy, Nephropathy and Neuropathy

by Dora Reglodi, Andrea Tamas, Inez Bosnyak, Tamas Atlasz, Edina Szabo, Lina Li, Gabriella Horvath, Balazs Opper, Peter Kiss, Liliana Lucas, Grazia Maugeri, Agata Grazia D’Amico, Velia D’Agata, Eszter Fabian, Gyongyver Reman and Alexandra Vaczy

Int. J. Mol. Sci. 2025, 26(19), 9650; https://doi.org/10.3390/ijms26199650 - 3 Oct 2025

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Abstract

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide exerting, among others, strong trophic and protective effects. It plays a role in several physiological functions, including glucose homeostasis. The protective effects of PACAP are mainly mediated via its specific PAC1 receptor by stimulating anti-inflammatory, anti-apoptotic and antioxidant pathways. The aim of the present review is to summarize data on the protective effects of PACAP in the three major complications of diabetes, retinopathy, nephropathy and neuropathy, as well as some other complications. In type 1 and type 2 diabetic retinopathy models and in glucose-exposed cells of the eye, PACAP counteracted the degeneration of retinal layers and inhibited apoptosis and factors leading to abnormal vessel growth. In models of nephropathy, kidney morphology was better retained after PACAP administration, with decreased apoptosis and fibrosis. In diabetic neuropathy, PACAP protected against axonal–myelin lesions and less activation in pain processing centers. This neuropeptide has several other beneficial effects in diabetes-induced complications like altered vascular response, cognitive deficits and atherosclerosis. The promising therapeutic effects of PACAP in several pathological conditions have encouraged researchers to design PACAP-related drugs and to develop ways to enhance tissue delivery. These intentions are expected to result in overcoming the hurdles preventing PACAP from being introduced into therapeutic treatments, including diabetes-related conditions. Full article

(This article belongs to the Special Issue Molecular Research on Type 1 Diabetes and Its Complications: 2nd Edition)

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