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Cells
Special Issues
Kidney Disease Models, Cellular Mechanism and Potential Treatment
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Kidney Disease Models, Cellular Mechanism and Potential Treatment

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

Deadline for manuscript submissions: closed (10 January 2025) | Viewed by 3339

Special Issue Editor

Prof. Dr. Nicole Endlich

E-Mail Website
Guest Editor
Institute for Anatomy and Cell Biology, University Medicine Greifswald, Greifswald, Germany
Interests: podocytes; kidney diseases; zebrafish model; glomerulus; microscopy; miRNA; actin cytoskeleton; mechanical stretch
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to collect the latest research in the field of renal disease models, with a focus  on exploring cellular mechanisms and potential treatment strategies. We invite researchers in the field to submit original research articles on the following topics:

  • Models of kidney disease: Manuscripts describing the development and characterization of various new or improved models of kidney disease, including animal models, cell culture systems and organoids. This may include models for acute kidney injury, chronic   kidney disease, diabetic nephropathy, autoimmune, glomerular disease and
  • Cellular mechanisms: Studies on the underlying cellular and molecular mechanisms that contribute to the pathogenesis of kidney disease. Submissions should elucidate the key cellular processes, signaling pathways and genetic factors involved in the development of kidney
  • Therapeutic strategies: Innovative therapeutic approaches and potential treatment options for kidney disease at the cellular and molecular levels. Manuscripts should address drug development, regenerative medicine and precision medicine to improve patient

Prof. Dr. Nicole Endlich
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 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • kidney disease
  • signaling pathways
  • therapy
  • biomarker
  • prevention

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

Published Papers (2 papers)

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Research

20 pages, 3581 KiB  
Article
MAGED2 Enhances Expression and Function of NCC at the Cell Surface via cAMP Signaling Under Hypoxia
by Aline Radi, Sadiq Nasrah, Michelle Auer, Aparna Renigunta, Stefanie Weber, Elie Seaayfan and Martin Kömhoff
Cells 2025, 14(3), 175; https://doi.org/10.3390/cells14030175 - 23 Jan 2025
Viewed by 1479
Abstract
Mutations in MAGED2 cause transient antenatal Bartter syndrome (tBS) characterized by excessive amounts of amniotic fluid due to impaired renal salt transport via NKCC2 and NCC, high perinatal mortality, and pre-term birth. Surprisingly, renal salt handling completely normalizes after birth. Previously, we demonstrated [...] Read more.
Mutations in MAGED2 cause transient antenatal Bartter syndrome (tBS) characterized by excessive amounts of amniotic fluid due to impaired renal salt transport via NKCC2 and NCC, high perinatal mortality, and pre-term birth. Surprisingly, renal salt handling completely normalizes after birth. Previously, we demonstrated that, under hypoxic conditions, MAGED2 depletion enhances endocytosis of GalphaS (Gαs), reducing adenylate cyclase (AC) activation and cAMP production. This impaired cAMP signaling likely contributes to the dysfunction of salt transporters NKCC2 and NCC, explaining salt wasting and the subsequent recovery with renal oxygenation after birth. In this study, we show that MAGED2 depletion significantly decreases both total cellular and plasma membrane NCC expression and activity. We further demonstrate that MAGED2 depletion disrupts NCC trafficking by reducing exocytosis, increasing endocytosis, and promoting lysosomal degradation via enhanced ubiquitination. Additionally, forskolin (FSK), which increases cAMP production by activating AC, rescues NCC expression and localization in MAGED2-depleted cells. Conversely, MAGED2 overexpression increases NCC expression and membrane localization, although this effect is diminished in Gαs-depleted cells, indicating that Gαs acts downstream of MAGED2. In summary, our findings reveal the essential role of MAGED2 in regulating NCC function and trafficking under hypoxic conditions, providing new insights into the mechanisms behind salt loss in tBS and identifying potential therapeutic targets. Full article
(This article belongs to the Special Issue Kidney Disease Models, Cellular Mechanism and Potential Treatment)
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17 pages, 5353 KiB  
Article
SARS-CoV-2 Spike Protein Amplifies the Immunogenicity of Healthy Renal Epithelium in the Presence of Renal Cell Carcinoma
by Maryna Somova, Stefan Simm, Jens Ehrhardt, Janosch Schoon, Martin Burchardt and Pedro Caetano Pinto
Cells 2024, 13(24), 2038; https://doi.org/10.3390/cells13242038 - 10 Dec 2024
Viewed by 1262
Abstract
Renal cell carcinoma (RCC) is the most common form of kidney cancer, known for its immune evasion and resistance to chemotherapy. Evidence indicates that the SARS-CoV-2 virus may worsen outcomes for RCC patients, as well as patients with diminished renal function. Evidence suggests [...] Read more.
Renal cell carcinoma (RCC) is the most common form of kidney cancer, known for its immune evasion and resistance to chemotherapy. Evidence indicates that the SARS-CoV-2 virus may worsen outcomes for RCC patients, as well as patients with diminished renal function. Evidence suggests that the SARS-CoV-2 virus may exacerbate outcomes in RCC patients and those with impaired renal function. This study explored the unidirectional effects of RCC cells and the SARS-CoV-2 spike protein (S protein) on human renal proximal tubule epithelial cells (RPTECs) using a microphysiological approach. We co-cultured RCC cells (Caki-1) with RPTEC and exposed them to the SARS-CoV-2 S protein under dynamic 3D conditions. The impact on metabolic activity, gene expression, immune secretions, and S protein internalization was evaluated. The SARS-CoV-2 S protein was internalized by RPTEC but poorly interacted with RCC cells. RPTECs exposed to RCC cells and the S protein exhibited upregulated expression of genes involved in immunogenic pathways, particularly those related to antigen processing and presentation via the major histocompatibility complex I (MHCI). Additionally, increased TNF-α secretion suggested a pro-inflammatory response. Metabolic shifts toward glycolysis were observed in RCC co-culture, while the presence of the S protein led to minor changes. The presence of RCC cells amplified the immune-modulatory effects of the SARS-CoV-2 S protein on the renal epithelium, potentially exacerbating renal inflammation and fostering tumor-supportive conditions. These findings suggest that COVID-19 infections can impact renal function in the presence of kidney cancer. Full article
(This article belongs to the Special Issue Kidney Disease Models, Cellular Mechanism and Potential Treatment)
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