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Novel Biomarkers and Therapeutic Strategies in Nephropathy

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 (30 September 2024) | Viewed by 2359

Special Issue Editors


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Guest Editor
Nephrology, Dialysis and Transplantation Unit, Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Rende, Italy
Interests: clinical nephrology; hemodialysis; kidney transplantation; dialysis; chronic renal failure; transplantation; renal; kidney; chronic kidney failure; peritoneal dialysis; renal disease; kidney disease; fibrosis; transplant immunology
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Guest Editor
Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, Italy
Interests: translational research in nephrology; transplant medicine; kidney disease; renal disease

Special Issue Information

Dear Colleagues,

We kindly invite you to contribute to the Special Issue “Novel Biomarkers and Therapeutic Strategies in Nephropathy”. The traditional biomarkers used in clinical practice for assessing kidney function (e.g., GFR, serum creatinine, proteinuria) have the limitation that they increase when the damage is advanced. The early identification of kidney damage by one or multiple specific biomarkers is an important unmet need in nephrology to prevent disease progression, select the most effective therapy, and improve patient survival. In addition, researching suitable biomarkers may help researchers identify new potential therapeutic targets and drugs.

In recent years, the advances in molecular biology techniques with the development of molecular analysis of biopsy samples, liquid biopsy, advances in second-generation sequencing, and multi-omics technologies combined with progress in computational bioinformatics, artificial intelligence, and systems biology have pushed forward the research in this field. In the future, integrating novel identified biomarkers with clinical practice will lead to the development of personalized medicine.

Original articles and comprehensive reviews that focus on this area of research are welcome. Since IJMS is a journal of molecular science, pure clinical or model studies will not be suitable for our journal. However, clinical or pure model submissions with biomolecular experiments are welcome.

Prof. Dr. Gianluigi Zaza
Dr. Simona Granata
Dr. Michele Provenzano
Guest Editors

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Keywords

  • prognostic biomarkers
  • kidney diseases
  • predictive biomarkers
  • nephrology
  • rare diseases
  • glomerulonephritis
  • epidemiology
  • translational research
  • biomarkers
  • omics
  • transcriptomics
  • proteomics
  • metabolomics

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Published Papers (3 papers)

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Research

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22 pages, 8566 KiB  
Article
Identification of Genes Associated with Familial Focal Segmental Glomerulosclerosis Through Transcriptomics and In Silico Analysis, Including RPL27, TUBB6, and PFDN5
by Anfal Hussain Mahmoud, Reem Sami Alhamidi, Burcu Yener Ilce, Alaa Mohamed Hamad, Nival Ali, Amjad Mahasneh, Iman M. Talaat, Abdelaziz Tlili and Rifat Hamoudi
Int. J. Mol. Sci. 2024, 25(21), 11659; https://doi.org/10.3390/ijms252111659 - 30 Oct 2024
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Abstract
Focal segmental glomerulosclerosis (FSGS) is a major cause of nephrotic syndrome and often leads to progressive kidney failure. Its varying clinical presentation suggests potential genetic diversity, requiring further molecular investigation. This study aims to elucidate some of the genetic and molecular mechanisms underlying [...] Read more.
Focal segmental glomerulosclerosis (FSGS) is a major cause of nephrotic syndrome and often leads to progressive kidney failure. Its varying clinical presentation suggests potential genetic diversity, requiring further molecular investigation. This study aims to elucidate some of the genetic and molecular mechanisms underlying FSGS. The study focuses on the use of bioinformatic analysis of gene expression data to identify genes associated with familial FSGS. A comprehensive in silico analysis was performed using the GSE99340 data set from Gene Expression Omnibus (GEO) comparing gene expression in glomerular and tubulointerstitial tissues from FSGS patients (n = 10) and Minimal Change Disease (MCD) patients (n = 8). These findings were validated using transcriptomics data obtained using RNA sequencing from FSGS (n = 3) and control samples (n = 3) from the UAE. Further validation was conducted using qRT-PCR on an independent FFPE cohort (FSGS, n = 6; MCD, n = 7) and saliva samples (FSGS, n = 3; Control, n = 7) from the UAE. Three genes (TUBB6, RPL27, and PFDN5) showed significant differential expression (p < 0.01) when comparing FSGS and MCD with healthy controls. These genes are associated with cell junction organization and synaptic pathways of the neuron, supporting the link between FSGS and the neural system. These genes can potentially be useful as diagnostic biomarkers for FSGS and to develop new treatment options. Full article
(This article belongs to the Special Issue Novel Biomarkers and Therapeutic Strategies in Nephropathy)
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17 pages, 4525 KiB  
Article
Proteomic Changes Induced by the Immunosuppressant Everolimus in Human Podocytes
by Maurizio Bruschi, Simona Granata, Giovanni Candiano, Andrea Petretto, Martina Bartolucci, Xhuliana Kajana, Sonia Spinelli, Alberto Verlato, Michele Provenzano and Gianluigi Zaza
Int. J. Mol. Sci. 2024, 25(13), 7336; https://doi.org/10.3390/ijms25137336 - 4 Jul 2024
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Abstract
mTOR inhibitors (mTOR-Is) may induce proteinuria in kidney transplant recipients through podocyte damage. However, the mechanism has only been partially defined. Total cell lysates and supernatants of immortalized human podocytes treated with different doses of everolimus (EVE) (10, 100, 200, and 500 nM) [...] Read more.
mTOR inhibitors (mTOR-Is) may induce proteinuria in kidney transplant recipients through podocyte damage. However, the mechanism has only been partially defined. Total cell lysates and supernatants of immortalized human podocytes treated with different doses of everolimus (EVE) (10, 100, 200, and 500 nM) for 24 h were subjected to mass spectrometry-based proteomics. Support vector machine and partial least squares discriminant analysis were used for data analysis. The results were validated in urine samples from 28 kidney transplant recipients receiving EVE as part of their immunosuppressive therapy. We identified more than 7000 differentially expressed proteins involved in several pathways, including kinases, cell cycle regulation, epithelial–mesenchymal transition, and protein synthesis, according to gene ontology. Among these, after statistical analysis, 65 showed an expression level significantly and directly correlated with EVE dosage. Polo-Like Kinase 1 (PLK1) content was increased, whereas osteopontin (SPP1) content was reduced in podocytes and supernatants in a dose-dependent manner and significantly correlated with EVE dose (p < 0.0001, FDR < 5%). Similar results were obtained in the urine of kidney transplant patients. This study analyzed the impact of different doses of mTOR-Is on podocytes, helping to understand not only the biological basis of their therapeutic effects but also the possible mechanisms underlying proteinuria. Full article
(This article belongs to the Special Issue Novel Biomarkers and Therapeutic Strategies in Nephropathy)
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Review

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14 pages, 1786 KiB  
Review
A Possible Link between Cell Plasticity and Renin Expression in the Collecting Duct: A Narrative Review
by Nicole Schary, Bayram Edemir and Vladimir T. Todorov
Int. J. Mol. Sci. 2024, 25(17), 9549; https://doi.org/10.3390/ijms25179549 - 3 Sep 2024
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Abstract
The hormone renin is produced in the kidney by the juxtaglomerular cells. It is the rate-limiting factor in the circulating renin–angiotensin–aldosterone system (RAAS), which contributes to electrolyte, water, and blood pressure homeostasis. In the kidneys, the distal tubule and the collecting duct are [...] Read more.
The hormone renin is produced in the kidney by the juxtaglomerular cells. It is the rate-limiting factor in the circulating renin–angiotensin–aldosterone system (RAAS), which contributes to electrolyte, water, and blood pressure homeostasis. In the kidneys, the distal tubule and the collecting duct are the key target segments for RAAS. The collecting duct is important for urine production and also for salt, water, and acid–base homeostasis. The critical functional role of the collecting duct is mediated by the principal and the intercalated cells and is regulated by different hormones like aldosterone and vasopressin. The collecting duct is not only a target for hormones but also a place of hormone production. It is accepted that renin is produced in the collecting duct at a low level. Several studies have described that the cells in the collecting duct exhibit plasticity properties because the ratio of principal to intercalated cells can change under specific circumstances. This narrative review focuses on two aspects of the collecting duct that remain somehow aside from mainstream research, namely the cell plasticity and the renin expression. We discuss the link between these collecting duct features, which we see as a promising area for future research given recent findings. Full article
(This article belongs to the Special Issue Novel Biomarkers and Therapeutic Strategies in Nephropathy)
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