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Cells
Special Issues
Diabetes-Induced Organ Damage: Cellular Mechanisms and Therapeutic Opportunities
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Diabetes-Induced Organ Damage: Cellular Mechanisms and Therapeutic Opportunities

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 7455

Special Issue Editor

Prof. Dr. Mohammed S. Razzaque

E-Mail Website
Guest Editor
Professor of Pathology, Department of Medical Education, School of Medicine, University of Texas (UTRGV), 1204 W Schunior Street, Edinburg, TX 78541, USA
Interests: pathomechanisms of renal injury; renal structural and functional
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Prolonged diabetes can lead to chronic complications and end-stage organ damage, affecting almost all the systems of the body, including the heart, eyes, kidneys, brain, blood vessels, digestive system, skin, sexual organs, teeth, gums, feet and nerves. The damage can involve both large (macrovascular) and small (microvascular) blood vessels, leading to fatal conditions such as heart attack, stroke, kidney failure, ocular disorders and neuronal damage. The severity and duration of diabetes play a major role in determining the extent of organ involvement and subsequent damage. Altered glucose homeostasis can lead to cellular stress and mitochondrial dysfunction, contributing to the evolvement of nephropathy, cardiomyopathy, neuropathy and retinopathy.

Therapeutic opportunities for diabetes encompass a wide range of approaches, including medications, stem cell therapy and targeting cellular events. Medications such as incretin mimetics, amylin analogs and GIP analogs have shown potential benefits for controlling diabetes. Additionally, recent developments in stem cell therapy offer a promising approach to addressing the disease and its complications. Targeting cellular events, such as senescent cells and the senescence-associated secretory phenotype (SASP), represents significant opportunities for delaying the progression of type 2 diabetes and its complications. Furthermore, pancreatic β-cell endoplasmic reticulum stress has been identified as a promising therapeutic approach for addressing dysregulated insulin hypersecretion in diabetes mellitus. These diverse therapeutic opportunities provide hope for the more effective and targeted management and treatment of diabetes and its associated complications. Despite progress in understanding the etiology of diabetic injuries, there are knowledge gaps on subcellular mechanisms and effective therapeutic strategies in diabetes-induced organ damage.

This Special Issue welcomes the submission of clinical and basic science research manuscripts related to a wide range of diabetic injuries and newer treatment approaches, emphasizing the cellular mechanisms underlying diabetes-induced organ damage, therapeutic opportunities for diabetes-induced organ damage and ways in which insulin resistance contributes to diabetes-induced organ damage.

The submission may encompass original manuscripts (unpublished research works) and updated reviews (of the existing literature). The aim is to provide a broad and holistic updated knowledge of structural and functional organ impairment mechanisms during the progression of diabetes.

Preliminary studies including the effects of the ongoing pandemic or repeated vaccination on diabetes are also welcome.

Prof. Dr. Mohammed S. Razzaque
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • diabetes mellitus
  • vascular lesions
  • nephropathy
  • cardiomyopathy
  • neuropathy
  • retinopathy
  • therapeutic opportunities

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Published Papers (3 papers)

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Research

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18 pages, 2435 KiB  
Article
Impact of High Glucose on Bone Collagenous Matrix Composition, Structure, and Organization: An Integrative Analysis Using an Ex Vivo Model
by Rita Araújo, Ricardo N. M. J. Páscoa, Raquel Bernardino and Pedro S. Gomes
Cells 2025, 14(2), 130; https://doi.org/10.3390/cells14020130 - 17 Jan 2025
Viewed by 539
Abstract
Diabetes mellitus is a widespread metabolic disorder linked to numerous systemic complications, including adverse effects on skeletal health, such as increased bone fragility and fracture risk. Emerging evidence suggests that high glucose may disrupt the extracellular matrix (ECM) of bone, potentially altering its [...] Read more.
Diabetes mellitus is a widespread metabolic disorder linked to numerous systemic complications, including adverse effects on skeletal health, such as increased bone fragility and fracture risk. Emerging evidence suggests that high glucose may disrupt the extracellular matrix (ECM) of bone, potentially altering its composition and organization. Collagen, the primary organic component of the ECM, is critical for maintaining structural integrity and biomechanical properties. However, definitive evidence and a comprehensive understanding of the molecular mechanisms through which high glucose impacts the ECM and collagen remain elusive. This study employed an ex vivo embryonic chicken femur model to investigate the effects of high glucose on the collagenous matrix. A comprehensive approach integrating histological evaluation, histomorphometry, ATR-FTIR spectroscopy, and proteomics was adopted to unravel structural, biochemical, and molecular changes in the ECM. Histomorphometric analysis revealed disrupted collagen fibril architecture, characterized by altered fibril diameter, alignment, and spatial organization. ATR-FTIR spectroscopy highlighted biochemical modifications, including non-enzymatic glycation that impaired collagen crosslinking and reduced matrix integrity. Proteomic profiling unveiled significant alterations in ECM composition and function, including downregulation of key collagen crosslinking enzymes and upregulation of inflammatory and coagulation pathways. High glucose profoundly disrupts the collagenous matrix of bone, weakening its structural integrity and organization. These findings emphasize the critical impact of high glucose environments on extracellular matrix composition and bone quality, offering insights into the mechanisms behind diabetic bone fragility and guiding future research toward targeted therapeutic strategies. Full article
(This article belongs to the Special Issue Diabetes-Induced Organ Damage: Cellular Mechanisms and Therapeutic Opportunities)
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24 pages, 18910 KiB  
Article
ADAMTS13 Improves Endothelial Function and Reduces Inflammation in Diabetic Retinopathy
by Ahmed M. Abu El-Asrar, Mohd I. Nawaz, Ajmal Ahmad, Mairaj Siddiquei, Eef Allegaert, Lowie Adyns, Lotte Vanbrabant, Priscilla W. Gikandi, Gert De Hertogh, Sofie Struyf and Ghislain Opdenakker
Cells 2025, 14(2), 85; https://doi.org/10.3390/cells14020085 - 9 Jan 2025
Viewed by 602
Abstract
The protease, a disintegrin and metalloproteinase with thrombospondin type 1 motif member 13 (ADAMTS13), known to cleave only the von Willebrand factor (VWF), has powerful regulatory effects on microvascular platelet adhesion, thrombosis, inflammation, and endothelial dysfunction. We study the protection against diabetes-induced retinal [...] Read more.
The protease, a disintegrin and metalloproteinase with thrombospondin type 1 motif member 13 (ADAMTS13), known to cleave only the von Willebrand factor (VWF), has powerful regulatory effects on microvascular platelet adhesion, thrombosis, inflammation, and endothelial dysfunction. We study the protection against diabetes-induced retinal injury in experimental rats by supplementation with recombinant ADAMTS13. We compare human epiretinal membranes and vitreous samples from nondiabetic subjects and patients with proliferative diabetic retinopathy (PDR) and extend in vitro analyses with the use of various immunodetection and spectrofluorimetric methods on rat retina and human retinal glial and endothelial cell cultures. Functional studies include the assessment of the blood–retinal barrier (BRB), cell adhesion, and in vitro angiogenesis. In epiretinal membranes, endothelial cells and monocytes/macrophages express ADAMTS13. The levels of VWF, the platelet marker CD41, ADAMTS13, and the biomarkers of endothelial cell injury soluble VE-cadherin and soluble syndecan-1 are increased in PDR vitreous. ADAMTS13 is downregulated in diabetic rat retinas. The intravitreal administration of ADAMTS13 attenuates diabetes-induced BRB breakdown, the downregulation of VE-cadherin and β-catenin, and the upregulation of VWF, CD41, phospho-ERK1/2, HMGB1, VCAM-1, and ICAM-1. In Müller cells, ADAMTS13 attenuates MCP-1, MMP-9, and ROS upregulation induced by diabetic mimetic conditions. In HRMECs, ADAMTS13 attenuates the shedding of the soluble VE-cadherin and soluble syndecan-1 and the levels of phospho-ERK1/2, MCP-1, fractalkine, and ROS induced by diabetic mimetic conditions, the upregulation of ICAM-1 and VCAM-1 elicited by TNF-α, the adherence of monocytes induced by TNF-α, and VEGF-induced migration of human retinal microvascular endothelial cells. Our findings suggest that enhancing ADAMTS13 levels in situ ameliorates diabetes-induced retinal inflammation and vascular dysfunction. Full article
(This article belongs to the Special Issue Diabetes-Induced Organ Damage: Cellular Mechanisms and Therapeutic Opportunities)
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Review

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15 pages, 2694 KiB  
Review
Zinc and Diabetes: A Connection between Micronutrient and Metabolism
by Rahnuma Ahmad, Ronald Shaju, Azeddine Atfi and Mohammed S. Razzaque
Cells 2024, 13(16), 1359; https://doi.org/10.3390/cells13161359 - 15 Aug 2024
Cited by 4 | Viewed by 5428
Abstract
Diabetes mellitus is a global health problem and a major contributor to mortality and morbidity. The management of this condition typically involves using oral antidiabetic medication, insulin, and appropriate dietary modifications, with a focus on macronutrient intake. However, several human studies have indicated [...] Read more.
Diabetes mellitus is a global health problem and a major contributor to mortality and morbidity. The management of this condition typically involves using oral antidiabetic medication, insulin, and appropriate dietary modifications, with a focus on macronutrient intake. However, several human studies have indicated that a deficiency in micronutrients, such as zinc, can be associated with insulin resistance as well as greater glucose intolerance. Zinc serves as a chemical messenger, acts as a cofactor to increase enzyme activity, and is involved in insulin formation, release, and storage. These diverse functions make zinc an important trace element for the regulation of blood glucose levels. Adequate zinc levels have also been shown to reduce the risk of developing diabetic complications. This review article explains the role of zinc in glucose metabolism and the effects of its inadequacy on the development, progression, and complications of diabetes mellitus. Furthermore, it describes the impact of zinc supplementation on preventing diabetes mellitus. The available information suggests that zinc has beneficial effects on the management of diabetic patients. Although additional large-scale randomized clinical trials are needed to establish zinc’s clinical utility further, efforts should be made to increase awareness of its potential benefits on human health and disease. Full article
(This article belongs to the Special Issue Diabetes-Induced Organ Damage: Cellular Mechanisms and Therapeutic Opportunities)
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