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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: 30 August 2024 | Viewed by 2379

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

Published Papers (3 papers)

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Research

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
Viewed by 517
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)
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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
Viewed by 490
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)
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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 921
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)
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