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Biomolecules
Special Issues
Molecular and Cellular Mechanisms of Kidney Diseases
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Molecular and Cellular Mechanisms of Kidney Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 October 2025) | Viewed by 5468

Special Issue Editors

Dr. Theodoros Eleftheriadis

E-Mail Website
Guest Editor
Professor of Nephrology, Department of Nephrology, Faculty of Medicine, University of Thessaly, Larissa, Greece
Interests: chronic kidney disease; acute kidney injury; kidney transplantation; glomerular diseases; ischemia–reperfusion injury; glucose toxicity; immunology
Special Issues, Collections and Topics in MDPI journals
Dr. Maria Divani

E-Mail Website
Guest Editor
Assistant Professor, Department of Nephrology, Faculty of Medicine, University of Thessaly, Larissa, Greece
Interests: chronic kidney disease; acute kidney injury; diabetic nephropathy; hypertension; glomerular diseases; ischemia–reperfusion injury

Special Issue Information

Dear Colleagues,

The global prevalence of chronic kidney disease (CKD) is estimated to exceed 10% and is on the rise, posing a significant challenge due to its detrimental effects on both quality of life and life expectancy. Concurrently, the incidence of acute kidney injury (AKI) remains high, particularly among hospitalized and critically ill patients, often resulting in poorer prognoses for these individuals.

Fortunately, extensive research over many years has led to the development of new diagnostic tools and therapeutic approaches for specific diseases contributing to CKD, especially various types of glomerulopathies, as well as strategies to decelerate CKD progression in general. Nevertheless, the residual risk remains high. Similar advancements have been made in the field of kidney transplantation; however, long-term kidney transplant survival has not significantly improved over the past decades. Efforts are also underway to facilitate earlier detection of AKI, although interventions targeting the molecular pathophysiology of AKI have not yet been widely implemented in clinical practice.

This Special Issue, titled "Molecular and Cellular Mechanisms of Kidney Diseases," invites authors to submit innovative reviews or original research articles on the mechanisms involved in the pathogenesis and complications of chronic kidney disease (CKD) and acute kidney injury (AKI). Additionally, we welcome translational articles that discuss the mechanisms of action of new or emerging therapies.

We look forward to receiving your contributions.

Dr. Theodoros Eleftheriadis
Dr. Maria Divani
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. Biomolecules is an international peer-reviewed open access monthly 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

  • chronic kidney disease
  • acute kidney injury
  • kidney transplantation
  • glomerular diseases
  • ischemia–reperfusion injury
  • diabetic nephropathy

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Published Papers (4 papers)

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Research

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14 pages, 619 KB  
Article
Inflammation and Dysregulated Bone Turnover Confound Serum ICAM-1 as a Cardiovascular Marker in Hemodialysis
by Maria Divani, Aikaterini Katsanaki, Panagiota Makri, Christina Poulianiti, Evangelos Lykotsetas, Andriani Balatsouka, Maria Tziastoudi, Ioannis Stefanidis and Theodoros Eleftheriadis
Biomolecules 2026, 16(1), 102; https://doi.org/10.3390/biom16010102 - 7 Jan 2026
Viewed by 790
Abstract
Cardiovascular disease (CVD) remains the leading cause of mortality among hemodialysis (HD) patients, underscoring the need for reliable biomarkers for early diagnosis and management. Serum intercellular adhesion molecule-1 (ICAM-1) has been investigated for years as a potential CVD marker but has yet to [...] Read more.
Cardiovascular disease (CVD) remains the leading cause of mortality among hemodialysis (HD) patients, underscoring the need for reliable biomarkers for early diagnosis and management. Serum intercellular adhesion molecule-1 (ICAM-1) has been investigated for years as a potential CVD marker but has yet to establish clinical utility. In a cohort of 142 HD patients, we examined the potential of serum ICAM-1 as a CVD biomarker and evaluated whether confounding factors, including low-grade inflammation and chronic kidney disease–mineral bone disorder (CKD-MBD), limit its diagnostic value. In addition to serum ICAM-1, routine biochemical parameters, bone alkaline phosphatase (bALP), and nitric oxide (NO) were measured. Serum levels of ICAM-1, bALP, and NO did not differ between patients with and without CVD, defined by a positive history of coronary heart disease, stroke, or peripheral arterial disease. Serum ICAM-1 concentrations were higher in HD patients with inflammation, as indicated by C-reactive protein levels >1 mg/dL. ICAM-1 showed no correlation with NO, a marker of endothelial dysfunction, but was positively correlated with bALP, a marker of CKD-MBD. In conclusion, serum ICAM-1 is not a reliable biomarker of CVD in HD patients. Its diagnostic utility appears confounded by inflammation and disturbances in bone turnover. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Kidney Diseases)
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21 pages, 1169 KB  
Article
Association of Oxidative Stress Markers with Cardio-Kidney-Metabolic Parameters and Cardiovascular Disease in Patients with Type 2 Diabetes Mellitus
by Stefanos Roumeliotis, Ioannis E. Neofytou, Athanasios Roumeliotis, Andrej Veljkovic, Milena Cojic and Gordana Kocic
Biomolecules 2026, 16(1), 42; https://doi.org/10.3390/biom16010042 - 26 Dec 2025
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Abstract
We aimed to investigate the association between oxidative stress (OS), inflammation, and kidney function and the predictive ability of OS for mortality and cardiovascular disease in 143 patients with type 2 diabetes (T2DM) and various degrees of kidney function. At baseline, we assessed [...] Read more.
We aimed to investigate the association between oxidative stress (OS), inflammation, and kidney function and the predictive ability of OS for mortality and cardiovascular disease in 143 patients with type 2 diabetes (T2DM) and various degrees of kidney function. At baseline, we assessed catalase, nitrogen oxides (NOx), malondialdehyde (MDA), advanced oxidation products (AOPPs), myeloperoxidase (MPO)], kidney function, and C-reactive protein (CRP). All patients were followed for 57 months, with the combined primary outcome of death/cardiovascular (CV) event, whichever occurred first. NOx was an independent predictor of estimated glomerular filtration rate (B = −0.097, p = 0.006), and MPO was correlated with glycated hemoglobin (r = 0.17, p = 0.046), CRP (r = −0.18, p = 0.032), and serum albumin (r = 0.2, p = 0.011, Spearman’s rho). During the follow-up, 24 composite events were documented. Kaplan–Meier curves showed that smoking (p = 0.029), serum albumin (p = 0.014), and MPO (p = 0.024, log-rank test) were associated with the outcome. In multivariate Cox regression models, smoking and MPO were independent predictors of the composite outcome (hazard ratio—HR = 2.8, p = 0.004, 955 confidence interval—CI 1.05–7.5 and HR = 0.99, p = 0.015, 95% CI: 0.98–1.00, respectively), after adjustment for several cofactors. OS might be associated with CV disease in T2DM. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Kidney Diseases)
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16 pages, 3007 KB  
Article
Modulators of Alpha-2 Macroglobulin Upregulation by High Glucose in Glomerular Mesangial Cells
by Jackie Trink, Renzhong Li, Bo Gao, Chao Lu and Joan C. Krepinsky
Biomolecules 2024, 14(11), 1444; https://doi.org/10.3390/biom14111444 - 13 Nov 2024
Cited by 4 | Viewed by 2327
Abstract
Up to 40% of patients with diabetes mellitus will develop diabetic kidney disease (DKD), characterized pathologically by the accumulation of extracellular matrix proteins, which leads to the loss of kidney function over time. Our previous studies showed that the pan-protease inhibitor alpha 2-macroglobulin [...] Read more.
Up to 40% of patients with diabetes mellitus will develop diabetic kidney disease (DKD), characterized pathologically by the accumulation of extracellular matrix proteins, which leads to the loss of kidney function over time. Our previous studies showed that the pan-protease inhibitor alpha 2-macroglobulin (A2M) is increased in DKD and is a critical regulator of the fibrotic response in glomerular mesangial cells (MC), an initial site of injury during DKD development. How A2M is regulated by high glucose (HG) has not yet been elucidated and is the focus of this investigation. Using serial deletions of the full A2M promoter, we identified the −405 bp region as HG-responsive in MC. Site-directed mutagenesis, siRNA, and ChIP studies showed that the transcription factor, nuclear factor of activated T cells 5 (NFAT5), regulated A2M promoter activity and protein expression in response to HG. Forkhead box P1 (FOXP1) served as a cooperative binding partner for NFAT5, required for A2M upregulation. Lastly, we showed that Smad3, known for its role in kidney fibrosis, regulated A2M promoter activity and protein production independently of HG. The importance of NFAT5, FOXP1, and Smad3 in A2M regulation was confirmed in ex vivo studies using isolated glomeruli. In conclusion, Smad3 is required for basal and HG-induced A2M expression, while NFAT5 and FOXP1 cooperatively regulate increased A2M transcription in response to HG. Inhibition of NFAT5/FOXP1 will be further evaluated as a potential therapeutic strategy to inhibit A2M production and attenuate profibrotic signaling in DKD. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Kidney Diseases)
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Review

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20 pages, 1050 KB  
Review
Signaling Pathways of the Acquired Immune System and Myocardial Dysfunction in Chronic Kidney Disease—What Do We Know So Far?
by Anila Duni, Christos Georgopoulos, Athanasios Kitsos, Georgios Markopoulos, Lefkothea Dova, Georgios Vartholomatos and Evangelia Dounousi
Biomolecules 2026, 16(1), 49; https://doi.org/10.3390/biom16010049 - 29 Dec 2025
Viewed by 705
Abstract
Aberrant signaling pathways of the acquired immune system are implicated in the development of cardiovascular disease (CVD) and chronic kidney disease (CKD) phenotypes. Understanding the complex abnormalities of lymphocyte subpopulations in CKD is a prerequisite for elucidating their implication in uremic cardiomyopathy. T [...] Read more.
Aberrant signaling pathways of the acquired immune system are implicated in the development of cardiovascular disease (CVD) and chronic kidney disease (CKD) phenotypes. Understanding the complex abnormalities of lymphocyte subpopulations in CKD is a prerequisite for elucidating their implication in uremic cardiomyopathy. T cell subsets display various patterns of association with indices of myocardial function in both experimental and clinical CKD models. The role of Tregs in CVD and CKD has attracted significant research interest. Although experimental data suggest a protective role of Tregs from the development of arterial hypertension- and pressure overload-induced myocardial hypertrophy, there might be a change in the regulatory T cell (Treg) phenotype towards a profibrotic one in the settings of CKD and heart failure. Depletion of B lymphocytes is a hallmark of CKD and heart failure, bearing adverse prognostic significance, yet evidence of B lymphocytes’ involvement in the pathogenesis of myocardial damage is currently lacking. Considering that myocardial remodeling is the final outcome of diverse pathogenic processes targeting the heart, the aim of this review is to present the evidence available up to now regarding the role of acquired immune cells in the pathogenesis of the structural and functional alterations of the myocardium in CKD. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Kidney Diseases)
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