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Molecular Mechanisms and Regulation in Chronic Kidney Diseases
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Molecular Mechanisms and Regulation in Chronic Kidney Diseases

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: 20 March 2025 | Viewed by 4930

Special Issue Editor

Prof. Dr. Marijn Speeckaert

E-Mail Website
Guest Editor
Department of Internal Medicine, Nephrology Division, Ghent University Hospital, 9000 Ghent, Belgium
Interests: biochemistry; biomarkers; hypertension; cardiovascular disease; kidney disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue focuses on exploring the intricate molecular mechanisms and regulatory pathways involved in chronic kidney disease (CKD). It gathers cutting-edge research that unveils new insights into the pathophysiology of CKD, emphasizing the role of molecular alterations in disease progression. The contributions cover a wide range of topics, including the identification of novel biomarkers, the role of genetic and epigenetic factors, and the impact of metabolic and inflammatory pathways in CKD. Significant attention is given to understanding how these molecular changes translate into clinical manifestations, thereby enhancing the potential for targeted therapeutic interventions. This Special Issue also highlights advances in diagnostic techniques, offering a more precise understanding of molecular changes in CKD. Overall, this Special Issue aims to gain a deeper understanding of CKD at a molecular level, paving the way for improved treatment strategies and patient outcomes.

Kind regards,

Prof. Dr. Marijn Speeckaert
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. 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

  • chronic kidney disease
  • pathophysiology
  • genetic and epigenetic factors
  • metabolic and inflammatory pathways

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Published Papers (4 papers)

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Research

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32 pages, 15113 KiB  
Article
Evaluation of the Effect of an α-Adrenergic Blocker, a PPAR-γ Receptor Agonist, and a Glycemic Regulator on Chronic Kidney Disease in Diabetic Rats
by Jorge Morones, Mariana Pérez, Martín Muñoz, Esperanza Sánchez, Manuel Ávila, Jorge Topete, Javier Ventura and Sandra Martínez
Int. J. Mol. Sci. 2024, 25(21), 11372; https://doi.org/10.3390/ijms252111372 - 23 Oct 2024
Viewed by 1086
Abstract
Diabetic nephropathy (DN) is a globally widespread complication of diabetes mellitus (DM). Research indicates that pioglitazone and linagliptin mitigate the risk of DN by reducing inflammation, oxidative stress, and fibrosis. The role of tamsulosin in DN is less studied, but it may contribute [...] Read more.
Diabetic nephropathy (DN) is a globally widespread complication of diabetes mellitus (DM). Research indicates that pioglitazone and linagliptin mitigate the risk of DN by reducing inflammation, oxidative stress, and fibrosis. The role of tamsulosin in DN is less studied, but it may contribute to reducing oxidative stress and inflammatory responses. The protective effects of combining pioglitazone, linagliptin, and tamsulosin on the kidneys have scarcely been investigated. This study examines the individual and combined effects of these drugs on DN in Wistar rats. Diabetic rats were treated with tamsulosin, pioglitazone, and linagliptin for six weeks. We assessed food and water intake, estimated glomerular filtration rate (eGFR), histological markers, urea, creatinine, glucose, NF-κB, IL-1, IL-10, TGF-β, and Col-IV using immunofluorescence and qPCR. The DN group exhibited hyperglycaemia, reduced eGFR, and tissue damage. Tamsulosin and linagliptin improved eGFR, decreased urinary glucose, and repaired tissue damage. Pioglitazone and its combinations restored serum and urinary markers and reduced tissue damage. Linagliptin lowered serum creatinine and tissue injury. In conclusion, tamsulosin, linagliptin, and pioglitazone demonstrated renoprotective effects in DN. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Regulation in Chronic Kidney Diseases)
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17 pages, 1303 KiB  
Article
Preclinical Detection of Early Glomerular Injury in Children with Kidney Diseases—Independently of Usual Markers of Kidney Impairment and Inflammation
by Heidrun Rhode, Baerbel Tautkus, Friederike Weigel, Julia Schitke, Oliver Metzing, Jan Boeckhaus, Wieland Kiess, Oliver Gross, Axel Dost and Ulrike John-Kroegel
Int. J. Mol. Sci. 2024, 25(17), 9320; https://doi.org/10.3390/ijms25179320 - 28 Aug 2024
Viewed by 735
Abstract
Glomerular kidney diseases typically begin insidiously and can progress to end stage kidney failure. Early onset of therapy can slow down disease progression. Early diagnosis is required to ensure such timely therapy. The goal of our study was to evaluate protein biomarkers (BMs) [...] Read more.
Glomerular kidney diseases typically begin insidiously and can progress to end stage kidney failure. Early onset of therapy can slow down disease progression. Early diagnosis is required to ensure such timely therapy. The goal of our study was to evaluate protein biomarkers (BMs) for common nephropathies that have been described for children with Alport syndrome. Nineteen candidate BMs were determined by commercial ELISA in children with congenital anomalies of the kidneys and urogenital tract, inflammatory kidney injury, or diabetes mellitus. It is particularly essential to search for kidney disease BMs in children because they are a crucial target group that likely exhibits early disease stages and in which misleading diseases unrelated to the kidney are rare. Only minor differences in blood between affected individuals and controls were found. However, in urine, several biomarker candidates alone or in combination seemed to be promising indicators of renal injury in early disease stages. The BMs of highest sensitivity and specificity were collagen type XIII, hyaluronan-binding protein 2, and complement C4-binding protein. These proteins are unrelated to inflammation markers or to risk factors for and signs of renal failure. In conclusion, our study evaluated several strong candidates for screening for early stages of kidney diseases and can help to establish early nephroprotective regimens. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Regulation in Chronic Kidney Diseases)
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Review

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19 pages, 975 KiB  
Review
Does the Composition of Gut Microbiota Affect Chronic Kidney Disease? Molecular Mechanisms Contributed to Decreasing Glomerular Filtration Rate
by Ewelina Młynarska, Emilian Budny, Maciej Saar, Ewa Wojtanowska, Justyna Jankowska, Szymon Marciszuk, Marcin Mazur, Jacek Rysz and Beata Franczyk
Int. J. Mol. Sci. 2024, 25(19), 10429; https://doi.org/10.3390/ijms251910429 - 27 Sep 2024
Viewed by 1423
Abstract
Chronic kidney disease (CKD) is a very prevalent and insidious disease, particularly with initially poorly manifested symptoms that progressively culminate in the manifestation of an advanced stage of the condition. The gradual impairment of kidney function, particularly decreased filtration capacity, results in the [...] Read more.
Chronic kidney disease (CKD) is a very prevalent and insidious disease, particularly with initially poorly manifested symptoms that progressively culminate in the manifestation of an advanced stage of the condition. The gradual impairment of kidney function, particularly decreased filtration capacity, results in the retention of uremic toxins and affects numerous molecular mechanisms within the body. The dysbiotic intestinal microbiome plays a crucial role in the accumulation of protein-bound uremic toxins such as p-cresol (pC), indoxyl sulfate (IS), and p-cresyl sulfate (p-CS) through the ongoing fermentation process. The described phenomenon leads to an elevated level of oxidative stress and inflammation, subsequently resulting in tissue damage and complications, particularly an increase in cardiovascular risk, representing the predominant cause of mortality in chronic kidney disease (CKD). Therefore, exploring methods to reduce uremic toxins is currently a pivotal therapeutic strategy aimed at reducing the risk of organ damage in patients with chronic kidney disease (CKD). This review aims to summarize recent discoveries on modifying the composition of the intestinal microbiota through the introduction of special probiotic and synbiotic supplements for CKD therapy. The potential to connect the gut microbiota with CKD opens the possibility for further extensive research in this area, which could lead to the incorporation of synbiotics and probiotics into the fundamental treatment and prevention of CKD. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Regulation in Chronic Kidney Diseases)
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21 pages, 832 KiB  
Review
Cyclic Adenosine Monophosphate Signaling in Chronic Kidney Disease: Molecular Targets and Therapeutic Potentials
by Charlotte Delrue, Reinhart Speeckaert, Rafael Noal Moresco and Marijn M. Speeckaert
Int. J. Mol. Sci. 2024, 25(17), 9441; https://doi.org/10.3390/ijms25179441 - 30 Aug 2024
Viewed by 1218
Abstract
Chronic kidney disease (CKD) is characterized by a steady decline in kidney function and affects roughly 10% of the world’s population. This review focuses on the critical function of cyclic adenosine monophosphate (cAMP) signaling in CKD, specifically how it influences both protective and [...] Read more.
Chronic kidney disease (CKD) is characterized by a steady decline in kidney function and affects roughly 10% of the world’s population. This review focuses on the critical function of cyclic adenosine monophosphate (cAMP) signaling in CKD, specifically how it influences both protective and pathogenic processes in the kidney. cAMP, a critical secondary messenger, controls a variety of cellular functions, including transcription, metabolism, mitochondrial homeostasis, cell proliferation, and apoptosis. Its compartmentalization inside cellular microdomains ensures accurate signaling. In kidney physiology, cAMP is required for hormone-regulated activities, particularly in the collecting duct, where it promotes water reabsorption through vasopressin signaling. Several illnesses, including Fabry disease, renal cell carcinoma, nephrogenic diabetes insipidus, Bartter syndrome, Liddle syndrome, diabetic nephropathy, autosomal dominant polycystic kidney disease, and renal tubular acidosis, have been linked to dysfunction in the cAMP system. Both cAMP analogs and phosphodiesterase inhibitors have the potential to improve kidney function and reduce kidney damage. Future research should focus on developing targeted PDE inhibitors for the treatment of CKD. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Regulation in Chronic Kidney Diseases)
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