Immunometabolic Reprogramming in Diabetic Kidney Disease: The Interplay of Innate Immunity, Oxidative Stress, and Cellular Metabolism

A Special Issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 March 2027 | Viewed by 973

Editors

1. Department of Anatomy, Histology and Embryology, School of Medicine, University of Split, Šoltanska 2A, 21000 Split, Croatia
2. Center for Translational Research in Biomedicine, University of Split School of Medicine, Šoltanska 2A, 21000 Split, Croatia
Interests: developmental nephrology; embryonic organogenesis; quantitative multiplex immunofluorescence; transcriptomic data integration; renal fibrosis and tumor biology
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
1. Department of Anatomy, Histology and Embryology, School of Medicine, University of Split, Soltanska 2A, 21000 Split, Croatia
2. Center for Translational Research in Biomedicine, University of Split School of Medicine, Soltanska 2A, 21000 Split, Croatia
Interests: kidney; genetics; gene expression; molecular mechanisms; nephropathy; diabetic nephropathy; apoptosis and fibrosis in renal tissue

E-Mail
Guest Editor
1. Department of Anatomy, Histology and Embryology, School of Medicine, University of Split, Soltanska 2A, 21000 Split, Croatia
2. Center for Translational Research in Biomedicine, University of Split School of Medicine, Šoltanska 2A, 21000 Split, Croatia
Interests: kidney; kidney development; mouse knockout models; kidney diseases; CAKUT

Special Issue Information

Dear Colleagues,

Kidney disorders, particularly diabetic kidney disease (DKD), represent a growing global health burden, driven by complex interplays among metabolic dysregulation, innate immune activation, and oxidative stress. A deeper understanding of the immunometabolic reprogramming underlying these processes is essential for identifying early biomarkers and developing targeted therapies.

We are pleased to invite you to contribute to this Special Issue titled “Immunometabolic Reprogramming in Diabetic Kidney Disease: The Interplay of Innate Immunity, Oxidative Stress, and Cellular Metabolism”, which aims to explore how aberrant cellular metabolism intersects with immune and oxidative pathways to promote renal injury and fibrosis.

This Special Issue seeks original research articles, reviews, and perspectives that elucidate the signaling pathways, gene regulatory networks, and cellular interactions governing immunometabolic crosstalk in DKD. Topics of interest include mitochondrial dysfunction, metabolic reprogramming in renal and immune cells, inflammasome activation (e.g., NLRP3), redox imbalance, and the role of innate immunity in driving inflammation and fibrosis. We especially welcome studies employing innovative approaches such as single-cell and spatial transcriptomics, organoid models, CRISPR-based screening, and multi-omics integration to unravel novel mechanistic insights.

By gathering multidisciplinary research, this Issue aims to advance our understanding of how immunometabolic axes contribute to DKD pathogenesis and to inspire innovative diagnostic and therapeutic strategies.

Research areas may include (but are not limited to) the following:

  • Metabolic reprogramming in diabetic kidney injury and repair;
  • Innate immune signaling (e.g., TLRs, inflammasomes) in DKD; 
  • Oxidative stress and mitochondrial dysfunction in renal cells; 
  • Epigenetic and non-coding RNA-mediated regulation of immunometabolic pathways; 
  • Podocyte and tubulointerstitial metabolic adaptation in diabetes; 
  • Inflammatory-fibrotic crosstalk driven by immunometabolic perturbations; 
  • Novel biomarkers and therapeutic targets derived from immunometabolic studies; 
  • Application of multi-omics and systems biology in DKD mechanism research; 
  • Advanced model systems (e.g., organoids, spatial transcriptomics) for studying DKD. 

We look forward to receiving your contributions.

Dr. Nela Kelam
Dr. Sandra Kostić
Dr. Anita Racetin
Guest Editors

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 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-anonymized 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

  • diabetic kidney disease
  • immunometabolism
  • innate immunity
  • oxidative stress
  • metabolic reprogramming
  • inflammasome
  • renal fibrosis
  • mitochondrial dysfunction
  • non-coding RNAs
  • multi-omics integration

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

18 pages, 26081 KB  
Article
Changes in Expression of Syndecans and Heparan Sulfate Biosynthesis Enzymes in Short-Term Streptozotocin-Induced Diabetic Rat Kidneys
by Tanja Čujić, Anita Racetin, Natalija Filipović, Sandra Kostić, Nela Kelam, Petar Todorović and Katarina Vukojević
Cells 2026, 15(14), 1277; https://doi.org/10.3390/cells15141277 - 16 Jul 2026
Viewed by 453
Abstract
Background: The aim of this study was to determine the temporal expression patterns of syndecan family members (SDC1, SDC2, SDC4) and heparan sulfate biosynthesis enzymes (NDST1, NDST2) in kidneys of diabetic rats and age-matched controls. Methods: Male Sprague–Dawley rats received intraperitoneal streptozotocin (55 [...] Read more.
Background: The aim of this study was to determine the temporal expression patterns of syndecan family members (SDC1, SDC2, SDC4) and heparan sulfate biosynthesis enzymes (NDST1, NDST2) in kidneys of diabetic rats and age-matched controls. Methods: Male Sprague–Dawley rats received intraperitoneal streptozotocin (55 mg/kg; DM1 group) or citrate buffer (control group). Kidney samples were harvested after 2 weeks and 2 months and processed for immunofluorescence. Results: SDC1 showed significant temporal upregulation in controls that was abolished in diabetic animals. SDC2 exhibited high early expression in the control group with significant decline as the kidneys matured but remained elevated in diabetic kidneys at 2 months compared to controls. SDC4 showed no significant difference between groups, though an age-related decrease was observed in controls. NDST1 was significantly upregulated in diabetic rats at 2 weeks, followed by profound suppression at 2 months (p < 0.0001). NDST2 showed modest but significant early elevation in diabetic animals. Transcript-level analysis of two independent public datasets of streptozotocin-induced diabetic rat renal cortex reproduced the principal directional findings—an early increase in SDC1 and a progressive elevation of SDC2—while indicating post-transcriptional regulation of SDC4 and the early NDST response. Conclusions: Diabetes disrupts normal temporal expression of syndecans and heparan sulfate biosynthesis enzymes in rat kidneys. Early compensatory upregulation of NDST1 and NDST2, followed by progressive NDST1 suppression, suggests a deteriorating heparan sulfate biosynthetic capacity, potentially contributing to the progression of diabetic nephropathy. Full article
Show Figures

Graphical abstract

Back to TopTop