Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
6.0
Journals
Cells
Special Issues
Metabolic Dysfunction and Kidney Diseases: Breakthroughs in Disease Management
share announcement

Metabolic Dysfunction and Kidney Diseases: Breakthroughs in Disease Management

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 22583

Special Issue Editor

Prof. Dr. Giuseppe Remuzzi

grade E-Mail Website
Guest Editor
Department of Rare Diseases, Negri Institute for Pharmacological Research, 24126 Bergamo, Italy
Interests: glomerulonephritis; kidney diseases; kidney transplantation; chronic kidney diseases; kidney regeneration

Special Issue Information

Dear Colleagues,

Chronic kidney disease (CKD) is a major global health concern that has high morbidity and mortality. The leading cause of kidney failure is diabetic kidney disease (DKD), which accounts for almost half of all incident cases in the Western world. On the other hand, obesity is one of the major causes of type 2 diabetes. Both of these metabolic diseases are associated with progressive kidney dysfunction, eventually leading to end-stage kidney disease (ESKD). Although glomerular hyperfiltration provides a potential pathogenic link between diabetes, obesity and CKD, the mechanisms underlying kidney disease and its progression in these settings remain to be further investigated in more depth. This will pave the way toward the development of novel therapeutic interventions that could potentially prevent or limit progressive kidney injury and loss of function.

This Special Issue will examine the recent advances in the pathophysiology of diabetes/obesity-associated chronic kidney injury in vitro and in vivo experimental models; current advances and challenges of RNA-based therapeutics (miRNAs), mesenchymal stromal cells from different sources and innovative drugs to counteract DKD in vivo models; and the evidence for the safety and renoprotection of cell-based therapies, novel antidiabetic drugs and novel cholesterol-lowering agents in diabetic/obese patients.

Prof. Dr. Giuseppe Remuzzi
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.

Published Papers (6 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

13 pages, 561 KiB  
Article
Resistin Contribution to Cardiovascular Risk in Chronic Kidney Disease Male Patients
by Katarzyna Romejko, Aleksandra Rymarz, Katarzyna Szamotulska, Zbigniew Bartoszewicz, Tomasz Rozmyslowicz and Stanisław Niemczyk
Cells 2023, 12(7), 999; https://doi.org/10.3390/cells12070999 - 24 Mar 2023
Cited by 2 | Viewed by 1325
Abstract
Background: Resistin is a molecule that belongs to the Resistin-Like Molecules family (RELMs), the group of proteins taking part in inflammatory processes. Increased resistin concentrations are observed in cardiovascular complications. Resistin contributes to the onset of atherosclerosis and intensifies the atherosclerotic processes. The [...] Read more.
Background: Resistin is a molecule that belongs to the Resistin-Like Molecules family (RELMs), the group of proteins taking part in inflammatory processes. Increased resistin concentrations are observed in cardiovascular complications. Resistin contributes to the onset of atherosclerosis and intensifies the atherosclerotic processes. The aim of this study was to investigate the relationship between resistin and cardiovascular (CV) risk in men with chronic kidney disease (CKD) not treated with dialysis. Materials and Methods: One hundred and forty-two men were included in the study: 99 men with eGFR lower than 60 mL/min/1.73 m2 and 43 men with eGFR ≥ 60 mL/min/1.73 m2. CV risk was assessed. Serum resistin, tumor necrosis factor-alpha (TNF-alpha) and plasminogen activator inhibitor-1 (PAI-1) were measured among other biochemical parameters. Results: We observed that resistin concentrations were significantly higher in patients with CKD compared to individuals with eGFR ≥ 60 mL/min/1.73 m2 (p = 0.003). In CKD, after estimating the general linear model (GLM), we found that resistin is associated with CV risk (p = 0.026) and PAI-1 serum concentrations (0.012). The relationship of PAI-1 with resistin depends on the level of CV risk in CKD (p = 0.048). Conclusions: Resistin concentrations rise with the increase of CV risk in CKD patients and thus resistin may contribute to the progression of cardiovascular risk in this group of patients. The relationship between resistin and CV risk is modified by PAI-1 concentrations. Full article
(This article belongs to the Special Issue Metabolic Dysfunction and Kidney Diseases: Breakthroughs in Disease Management)
►▼ Show Figures

Figure 1

Review

Jump to: Research

14 pages, 2891 KiB  
Review
Slowing the Progression of Diabetic Kidney Disease
by Olivia Blazek and George L. Bakris
Cells 2023, 12(15), 1975; https://doi.org/10.3390/cells12151975 - 31 Jul 2023
Cited by 2 | Viewed by 3057
Abstract
Diabetes is the most frequent cause of kidney disease that progresses to end-stage renal disease worldwide, and diabetic kidney disease is significantly related to unfavorable cardiovascular outcomes. Since the 1990s, specific therapies have emerged and been approved to slow the progression of diabetic [...] Read more.
Diabetes is the most frequent cause of kidney disease that progresses to end-stage renal disease worldwide, and diabetic kidney disease is significantly related to unfavorable cardiovascular outcomes. Since the 1990s, specific therapies have emerged and been approved to slow the progression of diabetic kidney disease, namely, renin–angiotensin–aldosterone system blockers (including angiotensin-converting enzyme inhibitors (ACEi) angiotensin receptor blockers (ARBs), the non-steroidal mineralocorticoid receptor antagonist (NS-MRA), finerenone, and sodium–glucose cotransporter-2 (SGLT2) inhibitors). Mechanistically, these different classes of agents bring different anti-inflammatory, anti-fibrotic, and complementary hemodynamic effects to patients with diabetic kidney disease such that they have additive benefits on slowing disease progression. Within the coming year, there will be data on renal outcomes using the glucagon-like peptide-1 receptor agonist, semaglutide. All the aforementioned medications have also been shown to improve cardiovascular outcomes. Thus, all three classes (maximally dosed ACEi or ARB, low-dose SGLT-2 inhibitors, and the NS-MRA, finerenone) form the “pillars of therapy” such that, when used together, they maximally slow diabetic kidney disease progression. Ongoing studies aim to expand these pillars with additional medications to potentially normalize the decline in kidney function and reduce associated cardiovascular mortality. Full article
(This article belongs to the Special Issue Metabolic Dysfunction and Kidney Diseases: Breakthroughs in Disease Management)
►▼ Show Figures

Figure 1

18 pages, 1197 KiB  
Review
Melatonin Treatment in Kidney Diseases
by Magdalena Markowska, Stanisław Niemczyk and Katarzyna Romejko
Cells 2023, 12(6), 838; https://doi.org/10.3390/cells12060838 - 08 Mar 2023
Cited by 7 | Viewed by 8786
Abstract
Melatonin is a neurohormone that is mainly secreted by the pineal gland. It coordinates the work of the superior biological clock and consequently affects many processes in the human body. Disorders of the waking and sleeping period result in nervous system imbalance and [...] Read more.
Melatonin is a neurohormone that is mainly secreted by the pineal gland. It coordinates the work of the superior biological clock and consequently affects many processes in the human body. Disorders of the waking and sleeping period result in nervous system imbalance and generate metabolic and endocrine derangements. The purpose of this review is to provide information regarding the potential benefits of melatonin use, particularly in kidney diseases. The impact on the cardiovascular system, diabetes, and homeostasis causes melatonin to be indirectly connected to kidney function and quality of life in people with chronic kidney disease. Moreover, there are numerous reports showing that melatonin plays a role as an antioxidant, free radical scavenger, and cytoprotective agent. This means that the supplementation of melatonin can be helpful in almost every type of kidney injury because inflammation, apoptosis, and oxidative stress occur, regardless of the mechanism. The administration of melatonin has a renoprotective effect and inhibits the progression of complications connected to renal failure. It is very important that exogenous melatonin supplementation is well tolerated and that the number of side effects caused by this type of treatment is low. Full article
(This article belongs to the Special Issue Metabolic Dysfunction and Kidney Diseases: Breakthroughs in Disease Management)
►▼ Show Figures

Figure 1

18 pages, 1341 KiB  
Review
Mitochondrial Contribution to Inflammation in Diabetic Kidney Disease
by Alla Mitrofanova, Antonio M. Fontanella, George W. Burke, Sandra Merscher and Alessia Fornoni
Cells 2022, 11(22), 3635; https://doi.org/10.3390/cells11223635 - 16 Nov 2022
Cited by 6 | Viewed by 2598
Abstract
Diabetes is the leading cause of chronic kidney disease worldwide. Despite the burden, the factors contributing to the development and progression of diabetic kidney disease (DKD) remain to be fully elucidated. In recent years, increasing evidence suggests that mitochondrial dysfunction is a pathological [...] Read more.
Diabetes is the leading cause of chronic kidney disease worldwide. Despite the burden, the factors contributing to the development and progression of diabetic kidney disease (DKD) remain to be fully elucidated. In recent years, increasing evidence suggests that mitochondrial dysfunction is a pathological mediator in DKD as the kidney is a highly metabolic organ rich in mitochondria. Furthermore, low grade chronic inflammation also contributes to the progression of DKD, and several inflammatory biomarkers have been reported as prognostic markers to risk-stratify patients for disease progression and all-cause mortality. Interestingly, the term “sterile inflammation” appears to be used in the context of DKD describing the development of intracellular inflammation in the absence of bacterial or viral pathogens. Therefore, a link between mitochondrial dysfunction and inflammation in DKD exists and is a hot topic in both basic research and clinical investigations. This review summarizes how mitochondria contribute to sterile inflammation in renal cells in DKD. Full article
(This article belongs to the Special Issue Metabolic Dysfunction and Kidney Diseases: Breakthroughs in Disease Management)
►▼ Show Figures

Figure 1

7 pages, 511 KiB  
Review
The Role of the Epidermal Growth Factor Receptor in Diabetic Kidney Disease
by Raymond C. Harris
Cells 2022, 11(21), 3416; https://doi.org/10.3390/cells11213416 - 28 Oct 2022
Cited by 5 | Viewed by 2415
Abstract
The epidermal growth factor receptor (EGFR) is expressed in numerous cell types in the adult mammalian kidney and is activated by a family of EGF-like ligands. EGFR activation has been implicated in a variety of physiologic and pathophysiologic functions. There is increasing evidence [...] Read more.
The epidermal growth factor receptor (EGFR) is expressed in numerous cell types in the adult mammalian kidney and is activated by a family of EGF-like ligands. EGFR activation has been implicated in a variety of physiologic and pathophysiologic functions. There is increasing evidence that aberrant EGFR activation is a mediator of progressive kidney injury in diabetic kidney disease. This review will highlight recent studies indicating its potential role and mechanisms of injury of both glomerular and tubular cells in development and progression of diabetic kidney disease. Full article
(This article belongs to the Special Issue Metabolic Dysfunction and Kidney Diseases: Breakthroughs in Disease Management)
►▼ Show Figures

Figure 1

19 pages, 606 KiB  
Review
The Contribution of Lipotoxicity to Diabetic Kidney Disease
by Jeffrey R. Schelling
Cells 2022, 11(20), 3236; https://doi.org/10.3390/cells11203236 - 14 Oct 2022
Cited by 15 | Viewed by 3782
Abstract
Lipotoxicity is a fundamental pathophysiologic mechanism in diabetes and non-alcoholic fatty liver disease and is now increasingly recognized in diabetic kidney disease (DKD) pathogenesis. This review highlights lipotoxicity pathways in the podocyte and proximal tubule cell, which are arguably the two most critical [...] Read more.
Lipotoxicity is a fundamental pathophysiologic mechanism in diabetes and non-alcoholic fatty liver disease and is now increasingly recognized in diabetic kidney disease (DKD) pathogenesis. This review highlights lipotoxicity pathways in the podocyte and proximal tubule cell, which are arguably the two most critical sites in the nephron for DKD. The discussion focuses on membrane transporters and lipid droplets, which represent potential therapeutic targets, as well as current and developing pharmacologic approaches to reduce renal lipotoxicity. Full article
(This article belongs to the Special Issue Metabolic Dysfunction and Kidney Diseases: Breakthroughs in Disease Management)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-6
Back to TopTop