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Molecular Therapeutics for Diabetes and Related 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 March 2026 | Viewed by 26411

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Dr. Kota V. Ramana

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Department of Biomedical Sciences, Noorda College of Osteopathic Medicine, Provo, UT 84606, USA
Interests: oxidative stress-induced signal transduction mechanisms; pathophysiology of secondary diabetic complications; carcinogenesis; inflammatory complications; therapeutic development of small molecular inhibitors and antioxidants
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Dear Colleagues,

Diabetes poses a significant threat to global health, demanding attention due to its escalating prevalence and associated complications. Conventional treatments, such as insulin therapy, alongside newer glucose-lowering medications such as metformin, GLP-1 receptor agonists, SGLT-2 inhibitors, and insulin sensitizers, offer some effectiveness; however, they are also associated with some unwanted side effects, which necessitates the further exploration of novel therapeutic options. Worldwide, healthcare costs of this pathology increase every year, and there is a need to discover novel drug targets and molecular pathways for managing diabetes and its associated complications, such as diabetic nephropathy, retinopathy, neuropathy, and cardiovascular diseases. These targets not only promise to ameliorate diabetes but also offer avenues for mitigating the associated complications. Connecting these novel pathways will help to surpass the benefits of conventional therapies, thereby reducing the morbidity and mortality linked with diabetic complications. While recent preclinical studies have identified promising molecular pathways and targets, further clinical trials are needed in order to translate these findings into clinical practice. Additionally, research continues to explore means of reducing oxidative stress; enhancing antioxidant status; manipulating molecular and metabolic pathways using the innate immune response; and exploring microRNAs, stem cell therapy, and gene therapy as potential diagnostic and therapeutic tools. Thus, while conventional therapies remain crucial, the pursuit of novel molecular therapeutics holds promise regarding revolutionizing diabetes management and improving patient outcomes. This Special Issue aims to compile state-of-the-art insights into the role of novel molecular therapeutics in ameliorating diabetes and related complications and welcomes the submission of original research and review articles addressing all aspects of molecular and cellular pathways, therapeutic drug development, biomarker identification and verification, novel techniques, and computational, structural, and functional studies in the field of diabetes and its complications.

Dr. Kota V. Ramana
Guest Editor

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Keywords

diabetes
diabetes complications
molecular therapeutics
drug development
hyperglycemia
insulin resistance
cell signaling and oxidative stress

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Related Special Issue

Molecular Therapeutics for Diabetes and Related Complications in International Journal of Molecular Sciences (11 articles)

Published Papers (9 papers)

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Research

Jump to: Review

16 pages, 1790 KB

Open AccessArticle

The NFAT5–AR Axis Is Associated with Hyperosmolarity, Renal Dysfunction, and Neutrophil-Related Inflammatory Markers in Diabetic Retinopathy

by Fátima Sofía Magaña-Guerrero, Beatriz Buentello-Volante, Norma Angélica Magaña-Guerrero, Óscar Vivanco-Rojas, Alfredo Domínguez-López and Yonathan Garfias

Int. J. Mol. Sci. 2026, 27(2), 1102; https://doi.org/10.3390/ijms27021102 - 22 Jan 2026

Viewed by 42

Abstract

Diabetic retinopathy (DR) is a major microvascular complication of type 2 diabetes (T2D) and is strongly associated with chronic inflammation. Neutrophils contribute to this inflammatory milieu, and the hyperosmolar stress-responsive transcription factor NFAT5 and its downstream effector aldose reductase (AR) may play crucial roles in this process. NFAT5 regulates AR, which converts glucose to sorbitol; excessive sorbitol accumulation promotes endothelial and retinal cell damage. Given the links between NFAT5, metabolic stress and immune activation, dysregulation of the NFAT5–AR axis in neutrophils may contribute to DR pathophysiology. This study evaluated NFAT5 and AR expression in peripheral blood neutrophils from 150 individuals classified as nondiabetic (n = 50), T2D without DR (n = 50), or T2D with DR (n = 50). Clinical, metabolic, and ophthalmic assessments were performed, and neutrophils were isolated to quantify NFAT5 and AR via ELISA. Associations with renal function, plasma osmolarity (pOSM), and hematological inflammatory ratios (NLR, NMR, NPAR, and SII) were analyzed. T2D-DR subjects presented impaired renal parameters, increased pOSM, reduced eGFR, and elevated NLR and NPAR. NFAT5 and AR levels were significantly increased in T2D-DR neutrophils and correlated positively with pOSM and the inflammatory ratios, whereas NFAT5 correlated inversely with the eGFR. These findings suggest that activation of the NFAT5–AR pathway contributes to neutrophil-driven inflammatory and hyperosmolar dysregulation in T2D and may influence DR progression. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications, 2nd Edition)

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17 pages, 2279 KB

Open AccessArticle

Canagliflozin Promotes Structural and Functional Changes in Proximal Tubular Cell Mitochondria of Hypertensive–Diabetic Mice

by Mayra Trentin-Sonoda, Yan Burelle, Alex Gutsol, Robert L. Myette and Richard L. Hébert

Int. J. Mol. Sci. 2025, 26(24), 11988; https://doi.org/10.3390/ijms262411988 - 12 Dec 2025

Viewed by 430

Abstract

The kidneys have a high-energy demand, relying on great rates of mitochondrial oxidative phosphorylation. Excessive glucose in the tubules leads to defective fatty acid oxidation, playing a key role in tubular injury and diabetic kidney disease progression. Besides its glucose-lowering action, canagliflozin (CANA) promotes kidney protective effects. We aimed to investigate whether the demonstrated kidney protective effects are extended to mitochondrial function and remodeling in proximal tubular cells from hypertensive–diabetic mice. Four weeks after streptozocin (STZ) induction of type 1 diabetes in genetic hypertensive (Lin) mice, they were fed either CANA-infused chow or a regular diet for 1 week. CANA treatment reverted the albuminuric state in LinSTZ mice. In PTECs from male mice, CANA promoted a complex mitochondrial network with less spherical and more branched organelles, with evidence of increased fusion. Those improvements reflected on the mitochondria bioenergetics, where CANA treatment induced an augmented baseline and maximum respiration rate, ATP production, and mitochondria membrane potential in PTECs, compared to LinSTZ. In females, CANA produced a milder response, increasing the mitochondrial network without affecting bioenergetics. In conclusion, in vivo CANA treatment positively affects proximal tubular cells’ mitochondria in male hypertensive–diabetic mice with a minor impact in females. The improvement in mitochondrial function and structure might be key to the kidney-protective effects of CANA. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications, 2nd Edition)

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16 pages, 1583 KB

Open AccessArticle

Development of Norrin-Based Protein Therapeutic for Activation of Norrin-Wnt Signaling in Human Retinal Endothelial Cells

by Kenneth P. Mitton, Wendy A. Dailey, Steven Q. Krikor and Kimberly A. Drenser

Int. J. Mol. Sci. 2025, 26(23), 11340; https://doi.org/10.3390/ijms262311340 - 24 Nov 2025

Viewed by 484

Abstract

Norrin–Wnt signaling is essential for retinal vascular development and generation of the inner blood retinal barrier. Norrin itself is a potential therapeutic for retinal vascular repair. We explored the feasibility of producing a recombinant protein therapeutic based on human Norrin for intravitreal injection. Norrin^K86P production was tested using MBP fusion and non-tagged versions. FZD4 binding was evaluated by an ELISA, and the activation of AXIN2 gene expression in primary human retinal microvascular endothelial cells was measured by qPCR. Intravitreal injection was tested in the rat eye, evaluated by fluoresceine angiography, OCT, and ERG. MBP-tagged Norrin was resistant to HRV3C protease cleavage unless linker polypeptides were also incorporated. MBP–Norrin or cleaved MBP–Norrin also required refolding with disulfide reshuffling to generate FZD4-binding activity and to affect AXIN-2 gene expression. A production strategy based upon untagged Norrin^K86P refolded from bacterial inclusion bodies was selected. Intravitreal injection of Norrin^K86P did not affect retinal thickness nor retinal function, the latter monitored by the ERG A-wave and B-wave amplitudes. We concluded that MBP–Norrin, cleaved Norrin, and untagged Norrin from inclusion bodies display Norrin-like biological activity after refolding with disulfide reshuffling. The untagged, bacterial inclusion body process was selected for future large-scale bacterial fermentation. Norrin^K86P could be produced with Norrin-like biochemical and biological activities and was tolerated after intravitreal injection into the rat eye. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications, 2nd Edition)

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18 pages, 841 KB

Open AccessArticle

Effect of Cocoa Supplementation on the Biochemical and Clinical Profile and the Somatosensory Processing of Diabetic Peripheral and Autonomic Neuropathy: A Randomized Clinical Trial

by Rebeca Kababie-Ameo, Gabriela Gutiérrez-Salmeán, Luisa Fernanda Salinas-Hernández, Virgilio Eduardo Trujillo-Condes, Israel Ramírez-Sánchez and Carlos A. Cuellar

Int. J. Mol. Sci. 2025, 26(16), 8033; https://doi.org/10.3390/ijms26168033 - 20 Aug 2025

Viewed by 3629

Abstract

Peripheral and autonomic neuropathy are common in type 2 diabetes; they are associated with oxidative stress and inflammation. Cocoa, rich in polyphenols, may offer neuroprotective benefits. This study evaluated the effect of cocoa supplementation on the biochemical, clinical, and somatosensory profile of neuropathy in individuals with type 2 diabetes. A 12-week, double-blind controlled trial involved 39 subjects randomized to receive cocoa capsules (50 mg polyphenols) or placebo (methylcellulose). Evaluations included glycemic and lipid profiles, neutrophil/lymphocyte ratio, blood pressure, standardized questionnaires, anthropometric measurements, and the rate-dependent depression of the H-reflex. In the cocoa group, the Toronto score decreased by 2.63 points and the BEST score decreased by 1.45 points. In the placebo group, these reductions were 1.84 and 2.21 points, respectively. Neither difference was statistically significant between groups (p > 0.05). Quality-of-Life questionnaire score decreased by 9.2 points in the cocoa group, but without significant difference to the placebo group (p = 0.501). Fasting glucose and HbA1c levels decreased in the placebo group by 38 mg/dL (0.28%) but were not significantly different from the cocoa group (p > 0.05). No other intra- or inter-group differences were significant (p > 0.05). Cocoa supplementation did not show significant improvements over the placebo in the measured outcomes. Both groups showed persistent abnormalities in spinal somatosensory processing, with an RDD of the H-reflex ≥ 0.5. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications, 2nd Edition)

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23 pages, 24539 KB

Open AccessArticle

NPC86 Increases LncRNA Gas5 In Vivo to Improve Insulin Sensitivity and Metabolic Function in Diet-Induced Obese Diabetic Mouse Model

by Anna Kharitonova, Rekha S. Patel, Brenna Osborne, Meredith Krause-Hauch, Ashley Lui, Gitanjali Vidyarthi, Sihao Li, Jianfeng Cai and Niketa A. Patel

Int. J. Mol. Sci. 2025, 26(8), 3695; https://doi.org/10.3390/ijms26083695 - 14 Apr 2025

Cited by 1 | Viewed by 1424

Abstract

In the United States, an estimated 38 million individuals (10% of the population) have type 2 diabetes mellitus (T2D), while approximately 97.6 million adults (38%) have prediabetes. Long noncoding RNAs (lncRNAs) are critical regulators of gene expression and metabolism. We were the first to demonstrate that lncRNA Growth Arrest-Specific Transcript 5 (GAS5 (human)/gas5 (mouse)) is decreased in the serum of T2D patients and established GAS5 as a biomarker for T2D diagnosis and onset prediction, now validated by other groups. We further demonstrated that GAS5 depletion impaired glucose uptake, decreased insulin receptor levels, and inhibited insulin signaling in human adipocytes, highlighting its potential as a therapeutic target in T2D. To address this, we developed NPC86, a small-molecule compound that stabilizes GAS5 by disrupting its interaction with UPF-1, an RNA helicase involved in nonsense-mediated decay (NMD) that regulates RNA stability. NPC86 increased GAS5 and insulin receptor (IR) levels, enhanced insulin signaling, and improved glucose uptake in vitro. In this study, we tested the efficacy of NPC86 in vivo in a diet-induced obese diabetic (DIOD) mouse model, and NPC86 treatment elevated gas5 levels, improved glucose tolerance, and enhanced insulin sensitivity, with no observed toxicity or weight changes. A transcriptomics analysis of adipose tissue revealed the upregulation of insulin signaling and metabolic pathways, including oxidative phosphorylation and glycolysis, while inflammatory pathways were downregulated. These findings highlight NPC86’s therapeutic potential in T2D. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications, 2nd Edition)

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Review

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19 pages, 543 KB

Open AccessReview

The Effect of Diabetes Mellitus on Central Corneal Thickness Values: A Systematic Review and Meta-Analysis

by Arda Uzunoglu, Juan José Valenzuela-Fuenzalida, Karin Morales-Calderón, Isidora Aguilar-Aguirre, Alejandro Bruna-Mejias, Pablo Nova-Baeza, Mathias Orellana-Donoso, Gustavo Oyanedel-Amaro, Alejandra Suazo-Santibañez, Juan A. Sanchis-Gimeno, Jose E. León Rojas and Guinevere Granite

Int. J. Mol. Sci. 2025, 26(17), 8695; https://doi.org/10.3390/ijms26178695 - 6 Sep 2025

Cited by 1 | Viewed by 1698

Abstract

Diabetes mellitus (DM) is a chronic metabolic disorder that can induce systemic and ocular complications. Among the latter, an increase in central corneal thickness (CCT) has been reported, potentially affecting endothelial function and increasing the risk of ocular disease. This study aimed to determine the impact of DM on CCT and to assess its correlation with diabetes duration and glycosylated hemoglobin (HbA1c) levels. A systematic literature search was conducted in Web of Science (1980–2025) following a PICO-based strategy. Observational studies evaluating CCT in diabetic patients were included. Data were analyzed using a random-effects model. Statistical heterogeneity was assessed with χ² test, p values, and I² index. Publication bias was evaluated using Begg’s funnel plot and Egger’s regression test. Twenty-nine studies were included in the meta-analysis. Diabetic patients showed significantly higher CCT values compared to controls, particularly in those with long-standing DM (p < 0.001) and poor glycemic control (HbA1c, p < 0.001). Egger’s regression suggested an association between increasing CCT, disease duration, and HbA1c levels, while funnel plot asymmetry indicated potential publication bias. CCT appears to increase in patients with long-term DM and inadequate glycemic control. These findings highlight the relevance of CCT assessment as a potential indicator of corneal changes in diabetic patients. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications, 2nd Edition)

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21 pages, 537 KB

Open AccessReview

Quercetin as an Anti-Diabetic Agent in Rodents—Is It Worth Testing in Humans?

by Tomasz Szkudelski, Katarzyna Szkudelska and Aleksandra Łangowska

Int. J. Mol. Sci. 2025, 26(15), 7391; https://doi.org/10.3390/ijms26157391 - 31 Jul 2025

Viewed by 1996

Abstract

Quercetin is a biologically active flavonoid compound that exerts numerous beneficial effects in humans and animals, including anti-diabetic activity. Its action has been explored in rodent models of type 1 and type 2 diabetes. It was revealed that quercetin mitigated diabetes-related hormonal and metabolic disorders and reduced oxidative and inflammatory stress. Its anti-diabetic effects were associated with advantageous changes in the relevant enzymes and signaling molecules. Quercetin positively affected, among others, superoxide dismutase, catalase, glutathione peroxidase, glucose transporter-2, glucokinase, glucose-6-phosphatase, glycogen phosphorylase, glycogen synthase, glycogen synthase kinase-3β, phosphoenolpyruvate carboxykinase, silent information regulator-1, sterol regulatory element-binding protein-1, insulin receptor substrate 1, phosphoinositide 3-kinase, and protein kinase B. The available data support the conclusion that the action of quercetin was pleiotropic since it alleviates a wide range of diabetes-related disorders. Moreover, no side effects were observed during treatment with quercetin in rodents. Given that human diabetes affects a large part of the population worldwide, the results of animal studies encourage clinical trials to evaluate the potential of quercetin as an adjunct to pharmacological therapies. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications, 2nd Edition)

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19 pages, 2781 KB

Open AccessReview

From Control to Cure: Insights into the Synergy of Glycemic and Antibiotic Management in Modulating the Severity and Outcomes of Diabetic Foot Ulcers

by Idris Ajibola Omotosho, Noorasyikin Shamsuddin, Hasniza Zaman Huri, Wei Lim Chong and Inayat Ur Rehman

Int. J. Mol. Sci. 2025, 26(14), 6909; https://doi.org/10.3390/ijms26146909 - 18 Jul 2025

Cited by 5 | Viewed by 6074

Abstract

Diabetic foot ulcers (DFUs), which affect approximately 15% of individuals with diabetes mellitus (DM), result from complex molecular disturbances involving chronic hyperglycemia, immune dysfunction, and infection. At the molecular level, chronic hyperglycemia promotes the formation of advanced glycation end products (AGEs), activates the AGE-RAGE-NF-κB axis, increases oxidative stress, and impairs macrophage polarization from the pro-inflammatory M1 to the reparative M2 phenotype, collectively disrupting normal wound healing processes. The local wound environment is further worsened by antibiotic-resistant polymicrobial infections, which sustain inflammatory signaling and promote extracellular matrix degradation. The rising threat of antimicrobial resistance complicates infection management even further. Recent studies emphasize that optimal glycemic control using antihyperglycemic agents such as metformin, Glucagon-like Peptide 1 receptor agonists (GLP-1 receptor agonists), and Dipeptidyl Peptidase 4 enzyme inhibitors (DPP-4 inhibitors) improves overall metabolic balance. These agents also influence angiogenesis, inflammation, and tissue regeneration through pathways including AMP-activated protein kinase (AMPK), mechanistic target of rapamycin (mTOR), and vascular endothelial growth factor (VEGF) signaling. Evidence indicates that maintaining glycemic stability through continuous glucose monitoring (CGM) and adherence to antihyperglycemic treatment enhances antibiotic effectiveness by improving immune cell function and reducing bacterial virulence. This review consolidates current molecular evidence on the combined effects of glycemic and antibiotic therapies in DFUs. It advocates for an integrated approach that addresses both metabolic and microbial factors to restore wound homeostasis and minimize the risk of severe outcomes such as amputation. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications, 2nd Edition)

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30 pages, 1501 KB

Open AccessReview

Comparison of the Mediterranean Diet and Other Therapeutic Strategies in Metabolic Syndrome: A Systematic Review and Meta-Analysis

by Alejandro Bruna-Mejias, Jessica San Martin, Danna Arciniegas-Diaz, Trinidad Meneses-Caroca, Amelia Salamanca-Cerda, Antonia Beas-Gambi, Jessica Paola-Loaiza-Giraldo, Cynthia Ortiz-Ahumada, Pablo Nova-Baeza, Gustavo Oyanedel-Amaro, Mathias Orellana-Donoso, Alejandra Suazo-Santibáñez, Juan Sanchis-Gimeno and Juan José Valenzuela-Fuenzalida

Int. J. Mol. Sci. 2025, 26(12), 5887; https://doi.org/10.3390/ijms26125887 - 19 Jun 2025

Cited by 7 | Viewed by 9398

Abstract

The Mediterranean diet (MD) is one of the healthiest diets, high in fiber, antioxidants, and unsaturated fats. MD improves lipid profiles, reduces inflammation, controls blood pressure, decreases insulin resistance, and enhances the sensitivity to this hormone, lowering the risks of Metabolic syndrome (MS). MS is characterized by central obesity, hypertension, insulin resistance, and dyslipidemia, increasing the risk of cardiovascular disease and type II diabetes. The objective of this study was to know the effectiveness of the MD versus other treatments in patients with MS. A systematic search across multiple databases, Medline, Embase, Web of Science, Scopus, Google Scholar, and Cinahl, was conducted using keywords such as “Mediterranean diet”, “Mediterranean food”, “eat mediterranean”, “Metabolic syndrome”, and “x syndrome”. A total of 12 studies met the inclusion criteria. Mediterranean diet at different doses versus other diets or other treatments showed significant improvements in clinical parameters, including BMI (mean difference of −0.83 95% CI: −0.93 to −0.74; p < 0.00001),waist circumference (mean difference = −1.81, CI = −2.63 to −0.99, p < 0.00001) triglycerides (mean difference = −22.38, CI = −32.86 to −11.90, p < 0.00001), Glucose (mean difference = −4.28, CI = −7.64 to −0.93, p = 0.005) and, HOMA IR (mean difference = −0.72, CI = −0.78 to −0.65, p < 0.00001), and Insulin resistance (mean difference = −2.98, CI = −3.27 to −2.69, p < 0.00001), all of which improved, Although there were more outcomes, these are the most important changes for patients with metabolic syndrome. MD improves metabolic and cardiovascular health, but study heterogeneity limits the results’ generalizability. Because of that, further research is needed to standardize approaches and explore their mechanisms. MD should be part of an optimized strategy that includes education and physical activity. The strength of the evidence was very low according to the GRADE approach. Further research is needed to support the efficacy of the Mediterranean diet in patients with MS. Full article

(This article belongs to the Special Issue Molecular Therapeutics for Diabetes and Related Complications, 2nd Edition)

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