Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Cellular and Molecular Research of Kidney Diseases—2nd Edition
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Cellular and Molecular Research of Kidney Diseases—2nd Edition

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: closed (20 December 2024) | Viewed by 7795

Special Issue Editor

Prof. Dr. Marta Ruiz-Ortega

E-Mail Website
Guest Editor
Faculty of Medicine, Cellular and Molecular Biology in Renal and Vascular Pathology Laboratory, Universidad Autónoma de Madrid (UAM), Fundación Jimenez Diaz, Avda Reyes Católicos 2, 28040 Madrid, Spain
Interests: cardiovascular and renal diseases; inflammation; fibrosis; growth factor; molecular mechanism; novel therapeutic targets
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic kidney disease (CKD) represents a wide variety of diseases with different etiologies, including immunological, metabolic, genetic, vascular or mechanical-related complications, as well as an age-related disorder. CKD is the 5th predicted global cause of death by 2040, the fastest increase among major causes of death, after Alzheimer, revealing the importance of research in this area. Current CKD therapies are limited to harsh immunosuppression in some fast progressive diseases, as immune glomerulonephritis, as well as drugs blocking the renin angiotensin system aimed to control systemic blood pressure. Although, recent trials have reported promising results with SGLT2 inhibition, the majority of CKD patients still progress towards end-stage renal damage (ESRD) requiring renal replacement therapies, such as dialysis or transplantation.

Intensive research in this area includes investigation of cellular communication, phenotype changes, including those related to senescent phenotypes, novel mediators of kidney injury, epigenetic mechanisms, activation of signaling pathways, among others, showing the complexity of this field. Strategies to target resident glomerular or tubular damage, as well as immune cells have been proposed to ameliorate disease progression or even revert kidney damage. In spite of all available data, translation of new research into novel therapies in CKD is greatly lagging behind other disciplines.

We invite you to submit novel research about molecular and cellular mechanisms involved in kidney injury.

Prof. Dr. Marta Ruiz-Ortega
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.

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

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

Published Papers (3 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

11 pages, 945 KiB  
Article
FGF23 as a Potential Pathophysiological Factor in Peripheral Arterial Disease Associated with Chronic Kidney Disease
by Javier Donate-Correa, Ernesto Martín-Núñez, Carolina Hernández-Carballo, Ainhoa González-Luis, Carmen Mora-Fernández, Alberto Martín-Olivera, Sergio Rodríguez-Ramos, Purificación Cerro-López, Ángel López-Castillo, Alejandro Delgado-Molinos, Victoria Castro López-Tarruella and Juan F. Navarro-González
Int. J. Mol. Sci. 2024, 25(10), 5457; https://doi.org/10.3390/ijms25105457 - 17 May 2024
Cited by 3 | Viewed by 1896
Abstract
Fibroblast growth factor 23 (FGF23) levels are often elevated in chronic kidney disease (CKD). FGF23 and inflammation are common characteristics in CKD, and both are associated with worse disease progression and the occurrence of complications. The existence of an interaction between FGF23 and [...] Read more.
Fibroblast growth factor 23 (FGF23) levels are often elevated in chronic kidney disease (CKD). FGF23 and inflammation are common characteristics in CKD, and both are associated with worse disease progression and the occurrence of complications. The existence of an interaction between FGF23 and inflammation has been suggested, each of which influences the expression and activity of the other, leading to a vicious feedback loop with adverse outcomes, including cardiovascular disease and mortality. In this work, we determined circulating FGF23 levels in a group of patients with CKD stages 3 and 4 subjected to elective femoral endarterectomy due to established peripheral artery disease (PAD), a condition resulting from an athero-inflammatory process, and we studied its associations with different inflammatory markers and mediators. We evaluated its association with serum tumor necrosis factor (TNF)α, interleukin (IL) 6, and IL10, as well as with the gene expression levels of these parameters and A disintegrin and metalloproteinase domain-containing protein (ADAM) 17 in femoral vascular tissue and peripheral blood circulating cells (PBCCs). We also analyzed its association with serum concentrations of C-reactive protein (CRP), the systemic immune inflammation index (SII), and the neutrophil-to-lymphocyte ratio (NLR). Finally, we determined the vascular immunoreactivity of protein TNFα in a subgroup of patients. FGF23 concentrations were independently associated with circulating and PBCC mRNA levels of TNFα. Worst kidney function and diabetes were also found to be contributing to FGF23 levels. Patients with higher levels of FGF23 also had greater vascular immunoreactivity for TNFα. Full article
(This article belongs to the Special Issue Cellular and Molecular Research of Kidney Diseases—2nd Edition)
►▼ Show Figures

Figure 1

Review

Jump to: Research

31 pages, 1658 KiB  
Review
Targeting Inflammatory Imbalance in Chronic Kidney Disease: Focus on Anti-Inflammatory and Resolution Mediators
by Rosaria Margherita Rispoli, Ada Popolo, Vincenzo De Fabrizio, Roberta d’Emmanuele di Villa Bianca, Giuseppina Autore, Jesmond Dalli and Stefania Marzocco
Int. J. Mol. Sci. 2025, 26(7), 3072; https://doi.org/10.3390/ijms26073072 - 27 Mar 2025
Viewed by 729
Abstract
Chronic kidney disease (CKD) is a condition caused by the gradual decline of renal function that approximatively affects 10–12% of the world population, thus representing a public health priority. In CKD patients, chronic and systemic low-grade inflammation is observed, and it significantly contributes [...] Read more.
Chronic kidney disease (CKD) is a condition caused by the gradual decline of renal function that approximatively affects 10–12% of the world population, thus representing a public health priority. In CKD patients, chronic and systemic low-grade inflammation is observed, and it significantly contributes to disease development and progression, especially for patients with advanced disease. It also results in CKD-associated complications and increased mortality. The low-grade inflammation is due to different factors, such as the decline of glomerular filtration rate, increased immune system activation, reactive oxygen species release, and intestinal homeostasis. Therefore, the possibility to control chronic low-grade inflammation in CKD deserves great attention. In this review, we will examine the current possible pharmacological approaches to counteract the inflammatory state in CKD, focusing our attention both on the pro-inflammatory factors and the pro-resolving mediators involved in CKD inflammatory state. Full article
(This article belongs to the Special Issue Cellular and Molecular Research of Kidney Diseases—2nd Edition)
►▼ Show Figures

Graphical abstract

27 pages, 1596 KiB  
Review
Novel Aspects of the Immune Response Involved in the Peritoneal Damage in Chronic Kidney Disease Patients under Dialysis
by Flavia Trionfetti, Vanessa Marchant, Guadalupe T. González-Mateo, Edyta Kawka, Laura Márquez-Expósito, Alberto Ortiz, Manuel López-Cabrera, Marta Ruiz-Ortega and Raffaele Strippoli
Int. J. Mol. Sci. 2023, 24(6), 5763; https://doi.org/10.3390/ijms24065763 - 17 Mar 2023
Cited by 15 | Viewed by 4143
Abstract
Chronic kidney disease (CKD) incidence is growing worldwide, with a significant percentage of CKD patients reaching end-stage renal disease (ESRD) and requiring kidney replacement therapies (KRT). Peritoneal dialysis (PD) is a convenient KRT presenting benefices as home therapy. In PD patients, the peritoneum [...] Read more.
Chronic kidney disease (CKD) incidence is growing worldwide, with a significant percentage of CKD patients reaching end-stage renal disease (ESRD) and requiring kidney replacement therapies (KRT). Peritoneal dialysis (PD) is a convenient KRT presenting benefices as home therapy. In PD patients, the peritoneum is chronically exposed to PD fluids containing supraphysiologic concentrations of glucose or other osmotic agents, leading to the activation of cellular and molecular processes of damage, including inflammation and fibrosis. Importantly, peritonitis episodes enhance peritoneum inflammation status and accelerate peritoneal injury. Here, we review the role of immune cells in the damage of the peritoneal membrane (PM) by repeated exposure to PD fluids during KRT as well as by bacterial or viral infections. We also discuss the anti-inflammatory properties of current clinical treatments of CKD patients in KRT and their potential effect on preserving PM integrity. Finally, given the current importance of coronavirus disease 2019 (COVID-19) disease, we also analyze here the implications of this disease in CKD and KRT. Full article
(This article belongs to the Special Issue Cellular and Molecular Research of Kidney Diseases—2nd Edition)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop