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