Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Kidney Injury: From Molecular Basis to Therapies 3.0

Special Issue Editors
Special Issue Information
Related Special Issues
Published Papers

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 (31 January 2021) | Viewed by 36199

Share This Special Issue

Special Issue Editor

Dr. Keiko Hosohata

E-Mail Website
Guest Editor

Education and Research Center for Clinical Pharmacy, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki 569-1094, Japan
Interests: inflammation; reactive oxygen species; renal physiology; blood pressure regulation; biomarker; clinical pharmacology; toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

This Special Issue is a continuation of our previous Special Issue “Kidney Injury: From Molecular Basis to Therapies” and “Kidney Injury: From Molecular Basis to Therapies 2.0”.

"Kidney injury" occurs at various stages of kidney disease. Renal fibrosis from kidney injury is a common pathway for the progression to chronic kidney disease (CKD). Despite the significant burden of CKD, specific therapies to prevent its incidence and progression remain limited. Therefore, novel therapies to prevent the decline of kidney function are needed.

This Special Issue of the International Journal of Molecular Sciences will focus on "Kidney Injury: From Molecular Basis to Therapies". It will include papers investigating the pathological mechanisms of CKD and experimental and clinical studies examining potential treatments to attenuate kidney dysfunction. In addition, works exploring the progression from acute kidney injury to CKD are welcome.

You may choose our Joint Special Issue in Reports.

Dr. Keiko Hosohata
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.

Related Special Issues

Kidney Injury: From Molecular Basis to Therapies 3.0 in Reports
Kidney Injury: From Molecular Basis to Therapies 2.0 in International Journal of Molecular Sciences (18 articles)

Published Papers (6 papers)

Download All Papers

Research

Jump to: Review

18 pages, 7166 KiB

Open AccessArticle

Expression Pattern of α-Tubulin, Inversin and Its Target Dishevelled-1 and Morphology of Primary Cilia in Normal Human Kidney Development and Diseases

by Ivana Solic, Anita Racetin, Natalija Filipovic, Snjezana Mardesic, Ivana Bocina, Danica Galesic-Ljubanovic, Meri Glavina Durdov, Mirna Saraga-Babić and Katarina Vukojevic

Int. J. Mol. Sci. 2021, 22(7), 3500; https://doi.org/10.3390/ijms22073500 - 28 Mar 2021

Cited by 5 | Viewed by 3042

Abstract

The spatiotemporal expression of α-tubulin, inversin and dishevelled-1 (DVL-1) proteins associated with the Wnt-signaling pathway, and primary cilia morphology were analyzed in developing kidneys (14th–38th developmental weeks), healthy postnatal (1.5- and 7-years old) and pathologically changed human kidneys, including multicystic dysplastic kidneys (MCDK), focal segmental glomerulosclerosis (FSGS) and nephrotic syndrome of the Finnish type (CNF). The analysis was performed by double immunofluorescence, electron microscopy, semiquantitative and statistical methods. Cytoplasmic co-expression of α-tubulin, inversin and DVL-1 was observed in the proximal convoluted tubules (pct), distal convoluted tubules (dct) and glomeruli (g) of analyzed tissues. During kidney development, the overall expression of α-tubulin, inversin and DVL-1 decreased, while in the postnatal period slightly increased. The highest expressions of α-tubulin and inversin characterized dct and g, while high DVL-1 characterized pct. α-tubulin, inversin and DVL-1 expression pattern in MCDK, FSGS and CNF kidneys significantly differed from the healthy control. Compared to healthy kidneys, pathologically changed kidneys had dysmorphic primary cilia. Different expression dynamics of α-tubulin, inversin and DVL-1 during kidney development could indicate that switch between the canonical and noncanonical Wnt-signaling is essential for normal kidney morphogenesis. In contrast, their disturbed expression in pathological kidneys might be associated with abnormal primary cilia, leading to chronic kidney diseases. Full article

(This article belongs to the Special Issue Kidney Injury: From Molecular Basis to Therapies 3.0)

► Show Figures

Figure 1

20 pages, 4499 KiB

Open AccessArticle

Delayed Exercise Training Improves Obesity-Induced Chronic Kidney Disease by Activating AMPK Pathway in High-Fat Diet-Fed Mice

by Florian Juszczak, Maud Vlassembrouck, Olivia Botton, Thomas Zwakhals, Morgane Decarnoncle, Alexandra Tassin, Nathalie Caron and Anne-Emilie Declèves

Int. J. Mol. Sci. 2021, 22(1), 350; https://doi.org/10.3390/ijms22010350 - 31 Dec 2020

Cited by 10 | Viewed by 3616

Abstract

Exercise training is now recognized as an interesting therapeutic strategy in managing obesity and its related disorders. However, there is still a lack of knowledge about its impact on obesity-induced chronic kidney disease (CKD). Here, we investigated the effects of a delayed protocol of endurance exercise training (EET) as well as the underlying mechanism in obese mice presenting CKD. Mice fed a high-fat diet (HFD) or a low-fat diet (LFD) for 12 weeks were subsequently submitted to an 8-weeks EET protocol. Delayed treatment with EET in obese mice prevented body weight gain associated with a reduced calorie intake. EET intervention counteracted obesity-related disorders including glucose intolerance, insulin resistance, dyslipidaemia and hepatic steatosis. Moreover, our data demonstrated for the first time the beneficial effects of EET on obesity-induced CKD as evidenced by an improvement of obesity-related glomerulopathy, tubulo-interstitial fibrosis, inflammation and oxidative stress. EET also prevented renal lipid depositions in the proximal tubule. These results were associated with an improvement of the AMPK pathway by EET in renal tissue. AMPK-mediated phosphorylation of ACC and ULK-1 were particularly enhanced leading to increased fatty acid oxidation and autophagy improvement with EET in obese mice. Full article

(This article belongs to the Special Issue Kidney Injury: From Molecular Basis to Therapies 3.0)

► Show Figures

Figure 1

16 pages, 2865 KiB

Open AccessArticle

A Novel Formulation of Glucose-Sparing Peritoneal Dialysis Solutions with l-Carnitine Improves Biocompatibility on Human Mesothelial Cells

by Francesca Piccapane, Mario Bonomini, Giuseppe Castellano, Andrea Gerbino, Monica Carmosino, Maria Svelto, Arduino Arduini and Giuseppe Procino

Int. J. Mol. Sci. 2021, 22(1), 123; https://doi.org/10.3390/ijms22010123 - 24 Dec 2020

Cited by 13 | Viewed by 3123

Abstract

The main reason why peritoneal dialysis (PD) still has limited use in the management of patients with end-stage renal disease (ESRD) lies in the fact that the currently used glucose-based PD solutions are not completely biocompatible and determine, over time, the degeneration of the peritoneal membrane (PM) and consequent loss of ultrafiltration (UF). Here we evaluated the biocompatibility of a novel formulation of dialytic solutions, in which a substantial amount of glucose is replaced by two osmometabolic agents, xylitol and l-carnitine. The effect of this novel formulation on cell viability, the integrity of the mesothelial barrier and secretion of pro-inflammatory cytokines was evaluated on human mesothelial cells grown on cell culture inserts and exposed to the PD solution only at the apical side, mimicking the condition of a PD dwell. The results were compared to those obtained after exposure to a panel of dialytic solutions commonly used in clinical practice. We report here compelling evidence that this novel formulation shows better performance in terms of higher cell viability, better preservation of the integrity of the mesothelial layer and reduced release of pro-inflammatory cytokines. This new formulation could represent a step forward towards obtaining PD solutions with high biocompatibility. Full article

(This article belongs to the Special Issue Kidney Injury: From Molecular Basis to Therapies 3.0)

► Show Figures

Figure 1

Review

Jump to: Research

17 pages, 1073 KiB

Open AccessReview

Matrix Metalloproteinase-10 in Kidney Injury Repair and Disease

by Xiaoli Sun and Youhua Liu

Int. J. Mol. Sci. 2022, 23(4), 2131; https://doi.org/10.3390/ijms23042131 - 15 Feb 2022

Cited by 7 | Viewed by 2834

Abstract

Matrix metalloproteinase-10 (MMP-10) is a zinc-dependent endopeptidase with the ability to degrade a broad spectrum of extracellular matrices and other protein substrates. The expression of MMP-10 is induced in acute kidney injury (AKI) and chronic kidney disease (CKD), as well as in renal cell carcinoma (RCC). During the different stages of kidney injury, MMP-10 may exert distinct functions by cleaving various bioactive substrates including heparin-binding epidermal growth factor (HB-EGF), zonula occludens-1 (ZO-1), and pro-MMP-1, -7, -8, -9, -10, -13. Functionally, MMP-10 is reno-protective in AKI by promoting HB-EGF-mediated tubular repair and regeneration, whereas it aggravates podocyte dysfunction and proteinuria by disrupting glomerular filtration integrity via degrading ZO-1. MMP-10 is also involved in cancerous invasion and emerges as a promising therapeutic target in patients with RCC. As a secreted protein, MMP-10 could be detected in the circulation and presents an inverse correlation with renal function. Due to the structural similarities between MMP-10 and the other MMPs, development of specific inhibitors targeting MMP-10 is challenging. In this review, we summarize our current understanding of the role of MMP-10 in kidney diseases and discuss the potential mechanisms of its actions. Full article

(This article belongs to the Special Issue Kidney Injury: From Molecular Basis to Therapies 3.0)

► Show Figures

Figure 1

40 pages, 4407 KiB

Open AccessReview

New Potential Biomarkers for Chronic Kidney Disease Management—A Review of the Literature

by Irina Lousa, Flávio Reis, Idalina Beirão, Rui Alves, Luís Belo and Alice Santos-Silva

Int. J. Mol. Sci. 2021, 22(1), 43; https://doi.org/10.3390/ijms22010043 - 22 Dec 2020

Cited by 39 | Viewed by 7729

Abstract

The prevalence of chronic kidney disease (CKD) is increasing worldwide, and the mortality rate continues to be unacceptably high. The biomarkers currently used in clinical practice are considered relevant when there is already significant renal impairment compromising the early use of potentially successful therapeutic interventions. More sensitive and specific biomarkers to detect CKD earlier on and improve patients’ prognoses are an important unmet medical need. The aim of this review is to summarize the recent literature on new promising early CKD biomarkers of renal function, tubular lesions, endothelial dysfunction and inflammation, and on the auspicious findings from metabolomic studies in this field. Most of the studied biomarkers require further validation in large studies and in a broad range of populations in order to be implemented into routine CKD management. A panel of biomarkers, including earlier biomarkers of renal damage, seems to be a reasonable approach to be applied in clinical practice to allow earlier diagnosis and better disease characterization based on the underlying etiologic process. Full article

(This article belongs to the Special Issue Kidney Injury: From Molecular Basis to Therapies 3.0)

► Show Figures

Figure 1

25 pages, 1917 KiB

Open AccessReview

Molecular Mechanisms of SGLT2 Inhibitor on Cardiorenal Protection

by Yi-Chou Hou, Cai-Mei Zheng, Tzung-Hai Yen and Kuo-Cheng Lu

Int. J. Mol. Sci. 2020, 21(21), 7833; https://doi.org/10.3390/ijms21217833 - 22 Oct 2020

Cited by 47 | Viewed by 15200

Abstract

The development of sodium-glucose transporter 2 inhibitor (SGLT2i) broadens the therapeutic strategies in treating diabetes mellitus. By inhibiting sodium and glucose reabsorption from the proximal tubules, the improvement in insulin resistance and natriuresis improved the cardiovascular mortality in diabetes mellitus (DM) patients. It has been known that SGLT2i also provided renoprotection by lowering the intraglomerular hypertension by modulating the pre- and post- glomerular vascular tone. The application of SGLT2i also provided metabolic and hemodynamic benefits in molecular aspects. The recent DAPA-CKD trial and EMPEROR-Reduced trial provided clinical evidence of renal and cardiac protection, even in non-DM patients. Therefore, the aim of the review is to clarify the hemodynamic and metabolic modulation of SGLT2i from the molecular mechanism. Full article

(This article belongs to the Special Issue Kidney Injury: From Molecular Basis to Therapies 3.0)

► Show Figures