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Biomolecules
Special Issues
New Insights into Kidney Disease Development and Therapy Strategies
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New Insights into Kidney Disease Development and Therapy Strategies

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 May 2025 | Viewed by 3859

Special Issue Editors

Dr. José I. López

E-Mail Website
Guest Editor
Biobizkaia Health Research Institute, 48903 Barakaldo, Spain
Interests: translational uropathology; pathological diagnosis; basic fundamentals of tumor biology
Special Issues, Collections and Topics in MDPI journals
Dr. Claudia Manini

E-Mail Website
Guest Editor
Department of Pathology, San Giovanni Bosco Hospital, 10154 Turin, Italy
Interests: urogenital and neurosurgical pathology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Basic science and practical issues related to etiological factors, methodology of analysis, diagnostic criteria, and therapeutic advances of neoplastic and non-neoplastic renal diseases are welcomed in this Special Issue, from renal epithelial/non-epithelial tumors to hereditary diseases, transplantation-related disorders, and glomerulonephritis. The Issue intends to bring together the experience of very different fields and serve as a unified forum for basic researchers, urologists, nephrologists, oncologists, pathologists, radiologists, and other related specialties.

You may choose our Joint Special Issue in Cancers.

Dr. José I. López
Dr. Claudia Manini
Guest Editors

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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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.

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

Published Papers (3 papers)

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Research

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11 pages, 2646 KiB  
Article
HL156A, an AMP-Activated Protein Kinase Activator, Inhibits Cyst Growth in Autosomal Dominant Polycystic Kidney Disease
by Sujung Seo, Hyunho Kim, Jung-Taek Hwang, Jin Eop Kim, Jisu Kim, Sohyun Jeon, Young-jin Song, Kwang-ho Choi, Gwangeon Sim, Myunkyu Cho, Jong-woo Yoon and Hyunsuk Kim
Biomolecules 2024, 14(7), 806; https://doi.org/10.3390/biom14070806 - 7 Jul 2024
Viewed by 876
Abstract
Background: Autosomal dominant polycystic kidney disease (ADPKD) is the most prevalent genetic kidney disorder. While metformin has demonstrated the ability to inhibit cyst growth in animal models of ADPKD via activation of adenosine monophosphate-activated protein kinase (AMPK), its effectiveness in humans is limited [...] Read more.
Background: Autosomal dominant polycystic kidney disease (ADPKD) is the most prevalent genetic kidney disorder. While metformin has demonstrated the ability to inhibit cyst growth in animal models of ADPKD via activation of adenosine monophosphate-activated protein kinase (AMPK), its effectiveness in humans is limited due to its low potency. This study explored the impact of HL156A, a new and more potent AMPK activator, in a mouse model of ADPKD. Methods: To investigate whether HL156A inhibits the proliferation of renal cyst cells in ADPKD in vitro, exogenous human telomerase reverse transcriptase (hTERT)-immortalized renal cyst cells from ADPKD patients were treated with HL156A, and an MTT (dimethylthiazol-diphenyltetrazolium bromide) assay was performed. To assess the cyst-inhibitory effect of HL156A in vivo, we generated Pkd1 conditional knockout (KO) mice with aquaporin 2 (AQP2)-Cre, which selectively expresses Cre recombinase in the collecting duct. The effectiveness of HL156A in inhibiting cyst growth and improving renal function was confirmed by measuring the number of cysts and blood urea nitrogen (BUN) levels in the collecting duct-specific Pkd1 KO mice. Results: When cyst cells were treated with up to 20 µM of metformin or HL156A, HL156A reduced cell viability by 25% starting at a concentration of 5 µM, whereas metformin showed no effect. When AQP2-Cre male mice were crossed with Pkd1flox/flox female mice, and when AQP2-Cre female mice were crossed with Pkd1flox/flox male mice, the number of litters produced by both groups was comparable. In collecting duct-specific Pkd1 KO mice, HL156A was found to inhibit cyst growth, reducing both the number and size of cysts. Furthermore, it was confirmed that kidney function improved as HL156A treatment led to a reduction in elevated BUN levels. Lastly, it was observed that the increase in AMPK phosphorylation induced by HL156A decreased ERK phosphorylation and α-SMA expression. Conclusion: HL156A has potential as a drug that can restore kidney function in ADPKD patients by inhibiting cyst growth. Full article
(This article belongs to the Special Issue New Insights into Kidney Disease Development and Therapy Strategies)
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17 pages, 6916 KiB  
Article
CircInpp5b Ameliorates Renal Interstitial Fibrosis by Promoting the Lysosomal Degradation of DDX1
by Xi Fang, Chengyuan Tang, Dong Zeng, Yi Shan, Qianfang Liu, Xuemin Yin and Ying Li
Biomolecules 2024, 14(6), 613; https://doi.org/10.3390/biom14060613 - 23 May 2024
Viewed by 887
Abstract
Renal interstitial fibrosis (RIF) is a classic pathophysiological process of chronic kidney disease (CKD). However, the mechanisms underlying RIF remain unclear. The present study found that a novel circular RNA, cirInpp5b, might be involved in RIF by high-throughput sequencing. Subsequent experiments revealed that [...] Read more.
Renal interstitial fibrosis (RIF) is a classic pathophysiological process of chronic kidney disease (CKD). However, the mechanisms underlying RIF remain unclear. The present study found that a novel circular RNA, cirInpp5b, might be involved in RIF by high-throughput sequencing. Subsequent experiments revealed that circInpp5b was reduced in UUO mouse kidney tissues and TGF-β1-treated proximal tubular cells. The overexpression of circInpp5b inhibited RIF in UUO mice and prevented extracellular matrix (ECM) deposition in TGF-β1-treated proximal tubular cells. Furthermore, overexpression of circInpp5b down-regulated the protein level of DDX1. Mechanistically, circInpp5b bound to the DDX1 protein and promoted its lysosomal degradation. Collectively, the findings of our study demonstrate that circInpp5b ameliorates RIF by binding to the DDX1 protein and promoting its lysosomal degradation. Full article
(This article belongs to the Special Issue New Insights into Kidney Disease Development and Therapy Strategies)
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Review

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21 pages, 1391 KiB  
Review
Navigating the Evolving Landscape of Primary Hyperoxaluria: Traditional Management Defied by the Rise of Novel Molecular Drugs
by Yueqi Huang, Wei Zhu, Jia Zhou, Qiulin Huang and Guohua Zeng
Biomolecules 2024, 14(5), 511; https://doi.org/10.3390/biom14050511 - 23 Apr 2024
Viewed by 1555
Abstract
Primary hyperoxalurias (PHs) are inherited metabolic disorders marked by enzymatic cascade disruption, leading to excessive oxalate production that is subsequently excreted in the urine. Calcium oxalate deposition in the renal tubules and interstitium triggers renal injury, precipitating systemic oxalate build-up and subsequent secondary [...] Read more.
Primary hyperoxalurias (PHs) are inherited metabolic disorders marked by enzymatic cascade disruption, leading to excessive oxalate production that is subsequently excreted in the urine. Calcium oxalate deposition in the renal tubules and interstitium triggers renal injury, precipitating systemic oxalate build-up and subsequent secondary organ impairment. Recent explorations of novel therapeutic strategies have challenged and necessitated the reassessment of established management frameworks. The execution of diverse clinical trials across various medication classes has provided new insights and knowledge. With the evolution of PH treatments reaching a new milestone, prompt and accurate diagnosis is increasingly critical. Developing early, effective management and treatment plans is essential to improve the long-term quality of life for PH patients. Full article
(This article belongs to the Special Issue New Insights into Kidney Disease Development and Therapy Strategies)
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