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Cells
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Kidney Disease: The Role of Cellular Mechanisms in Renal Pathology
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Kidney Disease: The Role of Cellular Mechanisms in Renal Pathology

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

Deadline for manuscript submissions: 31 August 2026 | Viewed by 3164

Special Issue Editor

Dr. Jinu Kim

E-Mail Website
Guest Editor
1. Department of Anatomy, Jeju National University College of Medicine, Jeju 63243, Republic of Korea
2. Interdisciplinary Graduate Program in Advanced Convergence Technology & Science, Jeju National University, Jeju 63243, Republic of Korea
Interests: kidney fibrosis; acute kidney injury; renal denervation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The growing incidence of kidney diseases, including chronic kidney disease (CKD) and acute kidney injury (AKI), poses significant challenges to global health. Cellular mechanisms play a crucial role in the development and progression of these conditions. Understanding the cellular dynamics within the kidney, such as epithelial-to-mesenchymal transition (EMT), fibrosis, and inflammation, is vital for improving diagnosis and therapeutic strategies. This Special Issue will explore the molecular and cellular mechanisms that underlie renal pathology, with a particular focus on kidney fibrosis, cell death, repair processes, and regeneration.

Key topics will include the identification of key renal cell populations involved in injury and repair, the role of stem and progenitor cells in kidney regeneration, and the impact of metabolic and environmental factors on renal health. In addition, we will highlight advancements in cell-based models for studying kidney disease, innovative therapeutic approaches targeting cellular pathways, and in vivo models used to assess novel treatments for kidney injury and fibrosis. This Special Issue aims at providing a comprehensive overview of the cellular mechanisms driving kidney diseases, offering new insights into potential therapeutic interventions and clinical applications.

Dr. Jinu Kim
Guest Editor

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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

  • kidney fibrosis
  • acute kidney injury (AKI)
  • chronic kidney disease (CKD)
  • epithelial-to-mesenchymal transition (EMT)
  • renal cell populations
  • stem cell therapy
  • renal regeneration
  • inflammation in kidney disease
  • cell-based models
  • renal repair mechanisms

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Published Papers (3 papers)

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Research

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25 pages, 3625 KB  
Article
Checkpoint Imbalance in Primary Glomerulopathies: Comparative Insights into IgA Nephropathy and Membranoproliferative Glomerulonephritis
by Sebastian Mertowski, Paulina Mertowska, Milena Czosnek, Iwona Smarz-Widelska, Wojciech Załuska and Ewelina Grywalska
Cells 2025, 14(19), 1551; https://doi.org/10.3390/cells14191551 - 3 Oct 2025
Cited by 2 | Viewed by 1508
Abstract
Introduction: Primary glomerulopathies are immune-driven kidney diseases. IgA nephropathy (IgAN) and membranoproliferative glomerulonephritis (MPGN) are prevalent entities with a risk of chronic progression. Immune checkpoints, such as PD-1/PD-L1, CTLA-4/CD86, and CD200R/CD200, regulate activation and tolerance in T, B, and NK cells, and also [...] Read more.
Introduction: Primary glomerulopathies are immune-driven kidney diseases. IgA nephropathy (IgAN) and membranoproliferative glomerulonephritis (MPGN) are prevalent entities with a risk of chronic progression. Immune checkpoints, such as PD-1/PD-L1, CTLA-4/CD86, and CD200R/CD200, regulate activation and tolerance in T, B, and NK cells, and also exist in soluble forms, reflecting systemic immune balance. Objective: To compare immune checkpoint profiles in IgAN and MPGN versus healthy volunteers (HV) through surface expression, soluble serum levels, and PBMC transcripts, with attention to sex-related differences and diagnostic value assessed by ROC curves. Materials and Methods: Ninety age-matched subjects were studied: IgAN (n = 30), MPGN (n = 30), HV (n = 30). Flow cytometry evaluated checkpoint expression on CD4+/CD8+ T cells, CD19+ B cells, and NK cells. ELISA quantified sPD-1, sPD-L1, sCTLA-4, sCD86, sCD200, sCD200R; PBMC transcript levels were assessed. Group comparisons, sex stratification, and ROC analyses were performed. Results: Lymphocyte distributions were preserved, but IgAN patients showed anemia and impaired renal function, while MPGN patients had greater proteinuria and dyslipidemia. GN patients displayed increased PD-1/PD-L1 and CD200R/CD200, with reduced CTLA-4/CD86, compared to HV. Serum analysis revealed elevated sPD-1, sPD-L1, sCD200, sCD200R and decreased sCTLA-4, sCD86. PBMC transcripts paralleled these trends, with PD-1/PD-L1 mainly increased in MPGN. Sex had minimal impact. ROC analyses showed strong GN vs. HV discrimination by CD19+CTLA-4+, PD-1/PD-L1, and CD200/CD200R, but limited ability to separate IgAN from MPGN. Conclusions: IgAN and MPGN share a sex-independent checkpoint signature: PD-1/PD-L1 and CD200R/CD200 upregulation with CTLA-4/CD86 downregulation. CD19+, CTLA-4+, and soluble PD-1/PD-L1/CD200(R) emerge as promising biomarkers requiring further validation. Full article
(This article belongs to the Special Issue Kidney Disease: The Role of Cellular Mechanisms in Renal Pathology)
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Review

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20 pages, 1222 KB  
Review
Zinc Signaling in Acute Kidney Injury
by Svetlana Lebedeva, Yan Bravyy, Anna Beknazarova, Elena A. Smolyarchuk and Kerim Mutig
Cells 2026, 15(11), 1018; https://doi.org/10.3390/cells15111018 - 1 Jun 2026
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Abstract
Acute kidney injury (AKI) is a life-threatening event prevalent in hospitalized patients but also not rare among endurance sports athletes. Hypoxia, oxidative stress, and sterile inflammation are the key pathophysiological factors driving kidney damage in AKI. Zinc is an essential trace element required [...] Read more.
Acute kidney injury (AKI) is a life-threatening event prevalent in hospitalized patients but also not rare among endurance sports athletes. Hypoxia, oxidative stress, and sterile inflammation are the key pathophysiological factors driving kidney damage in AKI. Zinc is an essential trace element required for the intact function of approximately 3000 proteins (~10% of the human proteome), including over 300 enzymes for which zinc serves as a cofactor. Cell biological tasks of zinc signaling include adaptive responses to hypoxia and oxidative stress, as well as anti-inflammatory effects. The underlying molecular pathways involve modulation of hypoxia-inducible factor signaling, suppression of reactive oxygen species (ROS) generation, and inhibition of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), the latter being the major pro-inflammatory transcription factor. As a catalytic cofactor for the “classical” histone deacetylases, zinc is essential for epigenetic control of gene expression, thereby exerting further adaptive effects. Apart from the intracellular zinc signaling, extracellular zinc elicits cytoprotective and anti-inflammatory effects via the G Protein-Coupled Receptor 39 (GPR39). GPR39 activation by zinc binding may exert antioxidant and anti-inflammatory effects mediated by the zinc-finger protein A20 (TNFAIP3) and NF-κB suppression, followed by reduced production of pro-inflammatory cytokines such as tumor necrosis factor (TNF), interleukin-1β (IL-1β), and IL-6. At the same time, GPR39 signaling may stimulates the release of the anti-inflammatory cytokine IL-10, thus shifting the kidney tissue towards an anti-inflammatory milieu, promoting renal recovery. The present review focuses on the role of zinc in AKI to identify potential therapeutic strategies targeting zinc signaling for renoprotection and biomarker-based risk stratification. Full article
(This article belongs to the Special Issue Kidney Disease: The Role of Cellular Mechanisms in Renal Pathology)
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21 pages, 1391 KB  
Review
miRNAs in Glomerular Diseases: From Pathogenic Insight to Therapeutic Potential: A Narrative Review
by Mugurel Apetrii, Alexandru Dan Costache, Irina Iuliana Costache Enache, Luminita Voroneanu, Andreea Simona Covic, Mehmet Kanbay, Dragos Viorel Scripcariu and Adrian Covic
Cells 2026, 15(2), 94; https://doi.org/10.3390/cells15020094 - 6 Jan 2026
Viewed by 840
Abstract
This article explores the multifaceted role of micro-ribonucleic acids (RNAs) (miRNAs) as critical posttranscriptional regulators in renal physiology and disease, with a focus on their emerging significance in glomerulopathies. miRNAs, small endogenous noncoding RNAs, modulate gene expression by promoting messenger RNA degradation or [...] Read more.
This article explores the multifaceted role of micro-ribonucleic acids (RNAs) (miRNAs) as critical posttranscriptional regulators in renal physiology and disease, with a focus on their emerging significance in glomerulopathies. miRNAs, small endogenous noncoding RNAs, modulate gene expression by promoting messenger RNA degradation or inhibiting translation, thereby orchestrating essential cellular processes such as proliferation, differentiation, apoptosis, and stress responses. Recent advances have revealed that aberrant miRNA expression profiles are intricately linked to the pathogenesis and progression of various renal diseases, including acute kidney injury, chronic kidney disease, alloimmune injury in solid organ transplantation and glomerulonephritis. This review summarizes the pathogenic and protective roles of miRNAs in major glomerulopathies, discusses their potential as diagnostic and prognostic biomarkers, and outlines future directions for their integration into personalized therapeutic strategies. At the moment, it is not fully established whether some of these mechanisms are the primary pathogenic driver or a secondary response. Combining miRNAs with other molecular markers may further enhance diagnostic and predictive accuracy, facilitating clinical translation, while selective targeting of specific miRNAs at different stages of disease progression could offer promising therapeutic opportunities. Full article
(This article belongs to the Special Issue Kidney Disease: The Role of Cellular Mechanisms in Renal Pathology)
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