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
New Insights into the Molecular Mechanisms of Kidney Injury and...
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

New Insights into the Molecular Mechanisms of Kidney Injury and Repair 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 August 2024) | Viewed by 8470

Special Issue Editor

Prof. Dr. Tzong-Shyuan Lee

E-Mail Website
Guest Editor
Graduate Institute, Department of Physiology, College of Medicine, National Taiwan University, Taipei 10617, Taiwan
Interests: cell culture; cholesterol metabolism; atherosclerosis; reactive oxygen species; signaling; endothelial cell biology; endothelial dysfunction; angiogenesis; vascular biology; vascular diseases; macrophage-foam cells; cardiovascular physiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The kidneys are important organs responsible for clearing waste products, salts, and water from the human body. The main physiological functions of kidneys include excretion of wastes, reabsorption of vital nutrients, acid-base homeostasis, maintenance of electrolyte–water balance, and hormone secretion. When kidney function is reduced to less than 15% by acute or chronic insults, a variety of health problems can be caused, such as coagulation abnormalities, cardiovascular dysfunction, vascular calcification, cancer, and cognitive disorders. Repeated unresolved damage after acute or chronic kidney injury leads to maladaptive repair and accelerated renal fibrosis by inducing deregulation of redox homeostasis and inflammatory response, as well as the senescence and death of renal tubular cells. However, the cellular and molecular mechanisms underlying the pathology of kidney diseases are not fully understood. Currently, the treatment of kidney diseases is not optimal; unraveling the mechanisms underlying the pathogenesis of kidney diseases will help develop the new therapeutic strategy for the treatment of kidney diseases. To this end, we sincerely invite researchers to contribute their research works to the Special Issue, entitled "New Insights into the Molecular Mechanisms of Kidney Injury and Repair 2.0", which aims to provide a research platform for the collection of original research articles and the latest reviews which cover all aspects of kidney diseases.

Prof. Dr. Tzong-Shyuan Lee
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

  • kidney disease
  • inflammation
  • redox
  • senescence
  • cell death
  • fibrosis
  • signaling pathway
  • uremic syndrome
  • cardiorenal syndrome
  • gut–kidney axis

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.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

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

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

12 pages, 682 KiB  
Article
Relationship Between Serum Uromodulin as a Marker of Kidney Damage and Metabolic Status in Patients with Chronic Kidney Disease of Non-Diabetic Etiology
by Radmila Žeravica, Branislava Ilinčić, Dragan Burić, Ana Jakovljević, Veljko Crnobrnja, Dalibor Ilić and Marija Vukmirović Papuga
Int. J. Mol. Sci. 2024, 25(20), 11159; https://doi.org/10.3390/ijms252011159 - 17 Oct 2024
Viewed by 827
Abstract
Chronic kidney disease (CKD) is often associated with dyslipidemia, marked by lipid abnormalities that can worsen kidney function and increase cardiovascular risk. A promising biomarker for evaluating kidney function and metabolic status in chronic kidney disease (CKD) is serum uromodulin (sUmod). This study [...] Read more.
Chronic kidney disease (CKD) is often associated with dyslipidemia, marked by lipid abnormalities that can worsen kidney function and increase cardiovascular risk. A promising biomarker for evaluating kidney function and metabolic status in chronic kidney disease (CKD) is serum uromodulin (sUmod). This study sought to further investigate the relationship between sUmod levels and metabolic status in non-diabetic CKD patients. A sensitive ELISA method was used to determine sUmod levels in 90 adults with obstructive nephropathy and 30 healthy controls. Kidney function was assessed using the measured glomerular filtration rate (mGFR) through renal clearance of 99mTc-diethylenetriamine penta-acetic acid, along with cystatin C levels. Additionally, glycemic and lipid statuses were evaluated. sUmod concentrations showed a significant association with High-density lipoprotein (HDL) levels. Furthermore, CKD patients with lower sUmod levels had significantly lower Apolipoprotein A-I (Apo A-I) values compared to the control group. Significant predictors of lower sUmod concentrations identified in this study were higher glycemia (B = −15.939; p = 0.003) and lower HDL cholesterol levels (B = 20.588; p = 0.019). We conclude that, in addition to being significantly reduced in CKD patients, sUmod is a potential predictor of metabolic syndrome (MS) in this population. Lower sUmod concentrations, independent of mGFR, predict lower HDL cholesterol levels and higher glycemia values. Full article
(This article belongs to the Special Issue New Insights into the Molecular Mechanisms of Kidney Injury and Repair 2.0)
►▼ Show Figures

Figure 1

11 pages, 2562 KiB  
Article
Study on the Effects of Angiotensin Receptor/Neprilysin Inhibitors on Renal Haemodynamics in Healthy Dogs
by Mio Ishizaka, Yurika Yamamori, Huai-Hsun Hsu, Yuichi Miyagawa, Naoyuki Takemura and Mizuki Ogawa-Yasumura
Int. J. Mol. Sci. 2024, 25(11), 6169; https://doi.org/10.3390/ijms25116169 - 3 Jun 2024
Viewed by 1676
Abstract
An angiotensin receptor/neprilysin inhibitor (ARNI), a heart failure treatment, is a combination drug made up of sacubitril, a neprilysin inhibitor, and valsartan, a vascular receptor blocker. No human or veterinary studies regarding the effect of ARNI on renal haemodynamics in the absence of [...] Read more.
An angiotensin receptor/neprilysin inhibitor (ARNI), a heart failure treatment, is a combination drug made up of sacubitril, a neprilysin inhibitor, and valsartan, a vascular receptor blocker. No human or veterinary studies regarding the effect of ARNI on renal haemodynamics in the absence of cardiac or renal issues exist. Therefore, we investigated the effect of ARNI on renal haemodynamics in five healthy dogs. ARNI was administered to all five dogs at an oral dose of 20 mg/kg twice daily for 4 weeks. Renal haemodynamics were assessed on the day before ARNI administration (BL), on Day 7, and on Day 28. The glomerular filtration rate (GFR) significantly increased on Day 28 compared to BL and Day 7, whereas renal plasma flow increased on Day 7 and Day 28 compared to BL. Systolic blood pressure significantly decreased between BL and Day 28. Plasma atrial natriuretic peptide (ANP) concentrations increased on Day 7 compared to BL. Additionally, ANP concentrations increased on Day 28 in three of the five dogs. Different ANP concentrations were observed in the remaining two dogs. Both urine output volume and heart rate remained relatively stable and did not exhibit significant change. In conclusion, ARNI may enhance renal haemodynamics in healthy dogs. ARNI could be a valuable drug for treating both heart and kidney disease in dogs. Full article
(This article belongs to the Special Issue New Insights into the Molecular Mechanisms of Kidney Injury and Repair 2.0)
►▼ Show Figures

Figure 1

15 pages, 3191 KiB  
Article
Renal Expression and Localization of the Receptor for (Pro)renin and Its Ligands in Rodent Models of Diabetes, Metabolic Syndrome, and Age-Dependent Focal and Segmental Glomerulosclerosis
by Carla Iacobini, Martina Vitale, Federica Sentinelli, Jonida Haxhi, Giuseppe Pugliese and Stefano Menini
Int. J. Mol. Sci. 2024, 25(4), 2217; https://doi.org/10.3390/ijms25042217 - 12 Feb 2024
Cited by 1 | Viewed by 1248
Abstract
The (pro)renin receptor ((P)RR), a versatile protein found in various organs, including the kidney, is implicated in cardiometabolic conditions like diabetes, hypertension, and dyslipidemia, potentially contributing to organ damage. Importantly, changes in (pro)renin/(P)RR system localization during renal injury, a critical information base, remain [...] Read more.
The (pro)renin receptor ((P)RR), a versatile protein found in various organs, including the kidney, is implicated in cardiometabolic conditions like diabetes, hypertension, and dyslipidemia, potentially contributing to organ damage. Importantly, changes in (pro)renin/(P)RR system localization during renal injury, a critical information base, remain unexplored. This study investigates the expression and topographic localization of the full length (FL)-(P)RR, its ligands (renin and prorenin), and its target cyclooxygenase-2 and found that they are upregulated in three distinct animal models of renal injury. The protein expression of these targets, initially confined to specific tubular renal cell types in control animals, increases in renal injury models, extending to glomerular cells. (P)RR gene expression correlates with protein changes in a genetic model of focal and segmental glomerulosclerosis. However, in diabetic and high-fat-fed mice, (P)RR mRNA levels contradict FL-(P)RR immunoreactivity. Research on diabetic mice kidneys and human podocytes exposed to diabetic glucose levels suggests that this inconsistency may result from disrupted intracellular (P)RR processing, likely due to increased Munc18-1 interacting protein 3. It follows that changes in FL-(P)RR cellular content mechanisms are specific to renal disease etiology, emphasizing the need for consideration in future studies exploring this receptor’s involvement in renal damage of different origins. Full article
(This article belongs to the Special Issue New Insights into the Molecular Mechanisms of Kidney Injury and Repair 2.0)
►▼ Show Figures

Figure 1

17 pages, 5675 KiB  
Article
Normal Proteasome Function Is Needed to Prevent Kidney Graft Injury during Cold Storage Followed by Transplantation
by Dinesh Bhattarai, Seong-Ok Lee, Lee Ann MacMillan-Crow and Nirmala Parajuli
Int. J. Mol. Sci. 2024, 25(4), 2147; https://doi.org/10.3390/ijms25042147 - 10 Feb 2024
Cited by 1 | Viewed by 993
Abstract
Kidney transplantation is the preferred treatment for end-stage kidney disease (ESKD). However, there is a shortage of transplantable kidneys, and donor organs can be damaged by necessary cold storage (CS). Although CS improves the viability of kidneys from deceased donors, prolonged CS negatively [...] Read more.
Kidney transplantation is the preferred treatment for end-stage kidney disease (ESKD). However, there is a shortage of transplantable kidneys, and donor organs can be damaged by necessary cold storage (CS). Although CS improves the viability of kidneys from deceased donors, prolonged CS negatively affects transplantation outcomes. Previously, we reported that renal proteasome function decreased after rat kidneys underwent CS followed by transplantation (CS + Tx). Here, we investigated the mechanism underlying proteasome dysfunction and the role of the proteasome in kidney graft outcome using a rat model of CS + Tx. We found that the key proteasome subunits β5, α3, and Rpt6 are modified, and proteasome assembly is impaired. Specifically, we detected the modification and aggregation of Rpt6 after CS + Tx, and Rpt6 modification was reversed when renal extracts were treated with protein phosphatases. CS + Tx kidneys also displayed increased levels of nitrotyrosine, an indicator of peroxynitrite (a reactive oxygen species, ROS), compared to sham. Because the Rpt6 subunit appeared to aggregate, we investigated the effect of CS + Tx-mediated ROS (peroxynitrite) generation on renal proteasome assembly and function. We treated NRK cells with exogenous peroxynitrite and evaluated PAC1 (proteasome assembly chaperone), Rpt6, and β5. Peroxynitrite induced a dose-dependent decrease in PAC1 and β5, but Rpt6 was not affected (protein level or modification). Finally, serum creatinine increased when we inhibited the proteasome in transplanted donor rat kidneys (without CS), recapitulating the effects of CS + Tx. These findings underscore the effects of CS + Tx on renal proteasome subunit dysregulation and also highlight the significance of proteasome activity in maintaining graft function following CS + Tx. Full article
(This article belongs to the Special Issue New Insights into the Molecular Mechanisms of Kidney Injury and Repair 2.0)
►▼ Show Figures

Figure 1

11 pages, 5055 KiB  
Article
Dietary Potassium Supplementation Reduces Chronic Kidney Lesions Independent of Blood Pressure in Deoxycorticosterone-Acetate and High Sodium Chloride-Treated Mice
by Qing Wang, Stephan C. Schäfer, Jacques-Antoine Haefliger, Marc P. Maillard and Florian Alonso
Int. J. Mol. Sci. 2023, 24(23), 16858; https://doi.org/10.3390/ijms242316858 - 28 Nov 2023
Viewed by 1500
Abstract
We have previously shown that an excess of deoxycorticosterone acetate and high sodium chloride intake (DOCA/salt) in one-renin gene mice induces a high urinary Na/K ratio, hypokalemia, and cardiac and renal hypertrophy in the absence of hypertension. Dietary potassium supplementation prevents DOCA/salt-induced pathological [...] Read more.
We have previously shown that an excess of deoxycorticosterone acetate and high sodium chloride intake (DOCA/salt) in one-renin gene mice induces a high urinary Na/K ratio, hypokalemia, and cardiac and renal hypertrophy in the absence of hypertension. Dietary potassium supplementation prevents DOCA/salt-induced pathological processes. In the present study, we further study whether DOCA/salt-treated mice progressively develop chronic inflammation and fibrosis in the kidney and whether dietary potassium supplementation can reduce the DOCA/salt-induced renal pathological process. Results showed that (1) long-term DOCA/salt-treated one-renin gene mice developed severe kidney injuries including tubular/vascular hypertrophy, mesangial/interstitial/perivascular fibrosis, inflammation (lymphocyte’s immigration), proteinuria, and high serum creatinine in the absence of hypertension; (2) there were over-expressed mRNAs of plasminogen activator inhibitor-1 (PAI-1), fibronectin, collagen type I and III, interferon-inducible protein-10 (IP-10), monocyte chemotactic protein-1 (MCP1), transforming growth factor-β (TGF-β), tumor necrosis factor-alpha (TNF-α), osteopontin, Nuclear factor kappa B (NF-κB)/P65, and intercellular adhesion molecule (ICAM)-1; and (3) dietary potassium supplementation normalized urinary Na/K ratio, hypokalemia, proteinuria, and serum creatinine, reduced renal hypertrophy, inflammations, and fibrosis, and down-regulated mRNA expression of fibronectin, Col-I and III, TGF-β, TNF-α, osteopontin, and ICAM without changes in the blood pressure. The results provide new evidence that potassium and sodium may modulate proinflammatory and fibrotic genes, leading to chronic renal lesions independent of blood pressure. Full article
(This article belongs to the Special Issue New Insights into the Molecular Mechanisms of Kidney Injury and Repair 2.0)
►▼ Show Figures

Figure 1

Review

Jump to: Research

12 pages, 716 KiB  
Review
Early Diagnosis and Treatment of Kidney Injury: A Focus on Urine Protein
by Duanna Zeng, Bing Wang, Zheng Xiao, Xiongqin Wang, Xiyang Tang, Xinsheng Yao, Ping Wang, Meifang Li, Yi Dai and Xiean Yu
Int. J. Mol. Sci. 2024, 25(20), 11171; https://doi.org/10.3390/ijms252011171 - 17 Oct 2024
Viewed by 1211
Abstract
The kidney, an essential excretory organ of the body, performs a series of crucial physiological functions such as waste removal, maintenance of electrolyte and acid–base balance, and endocrine regulation. Due to its rich blood flow and high metabolic activity, the kidney is susceptible [...] Read more.
The kidney, an essential excretory organ of the body, performs a series of crucial physiological functions such as waste removal, maintenance of electrolyte and acid–base balance, and endocrine regulation. Due to its rich blood flow and high metabolic activity, the kidney is susceptible to damage. Currently, kidney injury is classified into acute kidney injury (AKI) and chronic kidney disease (CKD), both of which are associated with high rates of morbidity and mortality on a global scale. The current clinical diagnosis of renal injury relies on the assessment of renal filtration function using creatinine and urea nitrogen as “gold-standard” markers. However, the delayed response time, limited specificity, and reduced accuracy of creatinine and urea nitrogen in evaluating kidney injury have significantly hindered advancements in diagnostic methods for kidney injury. Urinary protein is widely utilized as a biomarker for the early diagnosis of kidney injury due to the selectivity of the glomerular filtration system determining whether proteins can pass through the filtration barrier based on their size and charge. Therefore, as a complex biological sample with varying charges and particle sizes, urinary protein is considered an ideal indicator for monitoring the progression of kidney disease. Exploring the relationship between urinary protein and the advancement of kidney injury based on differences in particle size and charge offers a new perspective for assessing and treating such injuries. Hence, we conducted a comprehensive review of 74 relevant studies to gain a thorough understanding of the physiological mechanism and significance of proteinuria production. The aim was to explore the challenges and opportunities in clinical urine protein detection, as well as to discuss strategies targeting glomerular filtration barriers in order to effectively reduce urine protein levels and treat kidney injury, which could provide a new perspective for identifying the progression of kidney injury. Full article
(This article belongs to the Special Issue New Insights into the Molecular Mechanisms of Kidney Injury and Repair 2.0)
►▼ 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