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Molecular Insights into Diabetic Nephropathy
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Molecular Insights into Diabetic Nephropathy

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: 30 June 2026 | Viewed by 1400

Special Issue Editor

Prof. Dr. Natalija Filipović

E-Mail Website
Guest Editor
Department of Anatomy, Histology and Embryology, University of Split School of Medicine, Šoltanska 2, 21000 Split, Croatia
Interests: kidney; blood pressure regulation; acute kidney injury; chronic kidney disease; diabetic nephropathy; CAKUT; renal carcinoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Diabetic kidney disease (DKD; diabetic nephropathy) is one of the most serious microvascular complications of diabetes mellitus, the leading cause of end-stage chronic kidney disease worldwide, and the principal diagnosis in more than 50% of individuals undergoing renal transplantation. Hyperglycemia and insulin resistance in diabetes lead to metabolic stress in different populations of renal cells, the most sensitive being podocytes, endothelial cells, and the epithelium of the proximal tubules. These changes result in mitochondrial dysfunction, oxidative stress, and the triggering of inflammatory pathways, eventually leading to cytoskeletal reorganization and fibrosis. While some aspects of the complex molecular processes underlying these pathophysiological processes are understood, the field still remains largely unexplored. Therefore, we encourage authors to submit original research and review articles focusing on the molecular underpinnings of diabetic kidney disease pathophysiology.

Prof. Dr. Natalija Filipović
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 250 words) can be sent to the Editorial Office for assessment.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • diabetic nephropathy
  • hyperglycemia
  • insulin resistance
  • oxidative stress
  • mitochondrial dysfunction
  • chronic kidney disease

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Published Papers (2 papers)

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Research

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20 pages, 17930 KB  
Article
Ultrastructural Characterization of Pannexin 1 Expression Along the Rat Nephron
by Ivana Bočina, Nives Kević, Ivana Restović, Leo Jerčić, Marinela Jelinčić Korčulanin, Katarina Vukojević and Natalija Filipović
Int. J. Mol. Sci. 2026, 27(4), 1640; https://doi.org/10.3390/ijms27041640 - 7 Feb 2026
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Abstract
Pannexins are transmembrane glycoproteins that share structural and functional similarities with the gap junction proteins innexins and connexins. They play a critical role in paracrine and intracellular signalling, including purinergic signalling via the release of extracellular ATP. The role of pannexins in renal [...] Read more.
Pannexins are transmembrane glycoproteins that share structural and functional similarities with the gap junction proteins innexins and connexins. They play a critical role in paracrine and intracellular signalling, including purinergic signalling via the release of extracellular ATP. The role of pannexins in renal function and the pathophysiology of renal diseases is being intensely studied. However, there are no data on the subcellular localization of pannexin 1 expression in the rat kidney. We studied the distribution of pannexin 1 in the rat kidney, combining light microscopy with immunofluorescent immunohistochemistry and transmission electron microscopy with immunogold pannexin labelling. We found strong expression of pannexin in glomerular podocytes, proximal tubules and collecting ducts; moderate expression in the endothelium of glomerular and peritubular capillaries; thin descending and thick ascending limbs of the loop of Henle; and weaker pannexin 1 expression in the distal tubular epithelium. We described the detailed ultrastructural localization of pannexin 1 expression. This is the first study describing the ultrastructural distribution of pannexin 1 in the rat kidney, one of the most used preclinical models in renal physiology and pathology research. These results provide previously missing data on the precise distribution of pannexin 1 in the rat kidney, which is a prerequisite for a proper understanding of its role in renal physiology and pathophysiology. Full article
(This article belongs to the Special Issue Molecular Insights into Diabetic Nephropathy)
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Review

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21 pages, 633 KB  
Review
The Gut–Kidney–Metabolic Axis: Impact of Gut-Derived Uremic Toxins on Insulin Resistance in Diabetic Kidney Disease
by Charlotte Delrue, Margaux Vinckier, Reinhart Speeckaert, Stefania Marzocco and Marijn M. Speeckaert
Int. J. Mol. Sci. 2026, 27(8), 3472; https://doi.org/10.3390/ijms27083472 - 13 Apr 2026
Viewed by 272
Abstract
Chronic kidney disease (CKD), especially diabetic kidney disease (DKD), is characterized not only by progressive loss of renal function but also by profound metabolic disturbances, including insulin resistance (IR). Emerging evidence implicates gut-derived uremic toxins as mediators linking intestinal dysbiosis to metabolic and [...] Read more.
Chronic kidney disease (CKD), especially diabetic kidney disease (DKD), is characterized not only by progressive loss of renal function but also by profound metabolic disturbances, including insulin resistance (IR). Emerging evidence implicates gut-derived uremic toxins as mediators linking intestinal dysbiosis to metabolic and renal injury. Several microbial metabolites, for example, indoxyl sulfate, p-cresyl sulfate, and trimethylamine-N-oxide, are known to accumulate in CKD due to decreased renal excretion and altered tubular secretion. In vitro and in vivo experiments indicate that these gut-derived nephrotoxins impair insulin signaling pathways in cells. This results in increased production of reactive oxygen species, activation of stress kinases, higher levels of inflammatory cytokines, and inhibitory serine phosphorylation of insulin receptor substrates. Consequently, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling is impaired, reducing cellular glucose uptake. At the same time, these toxins induce endothelial dysfunction and mitochondrial damage, not only causing systemic IR but also contributing to the progression of kidney disease. Observational data link higher plasma toxin levels with components of IR, rapid loss of renal function as measured by estimated glomerular filtration rate, and a high risk of cardiovascular events in CKD patients. Although causality in humans remains unproven, interventions targeting the microbiota, toxin binding, and oxidative stress pathways show promise. We propose an integrated gut–kidney–metabolic framework in which dysbiosis-driven toxin production may amplify IR and DKD progression. Full article
(This article belongs to the Special Issue Molecular Insights into Diabetic Nephropathy)
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