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Molecular Mechanisms and Treatment of Kidney Diseases
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Molecular Mechanisms and Treatment of Kidney Diseases

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 25 March 2027 | Viewed by 5963

Editor

Dr. Junyi Zhu

E-Mail Website
Guest Editor
School of Medicine, University of Maryland, Baltimore, MD 21201, USA
Interests: drosophila; podocyte; nephrotic syndrome; diabetic nephropathy; mitochondria; histone modification
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Kidney diseases, including nephrotic syndrome, chronic kidney disease, and acute kidney injury, pose a significant and growing global health burden. Despite extensive clinical research, the underlying molecular mechanisms remain incompletely understood. There is an urgent need to investigate how genetic, epigenetic, metabolic, and immune-related factors contribute to the onset and progression of these conditions. Advancing this knowledge is essential for developing effective, targeted treatments for diverse forms of kidney disease. This Special Issue aims to present original research, mechanistic insights, and innovative therapeutic strategies that collectively offer a comprehensive understanding of renal pathobiology at the molecular level. We invite contributions on novel signaling pathways, disease models, and translational biomarkers to advance personalized approaches for kidney disease prevention and treatment.

Dr. Junyi Zhu
Guest Editor

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Keywords

  • nephrotic syndrome
  • kidney disease
  • kidney injury

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Published Papers (5 papers)

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Research

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28 pages, 8275 KB  
Article
SUMOylation-Driven Subtype Heterogeneity and Prognostic Biomarkers in Renal Cell Carcinoma
by Xiaobo Zhang, Zhiming Li, Ruoxin Lin, Suping Yang, Xiaohui Sun and Shicheng Chen
Curr. Issues Mol. Biol. 2026, 48(8), 751; https://doi.org/10.3390/cimb48080751 - 23 Jul 2026
Viewed by 260
Abstract
Renal cell carcinoma (RCC) is the most common malignancy of the urinary system, characterized by high incidence, mortality, and resistance to therapy. Its molecular heterogeneity presents challenges for effective precision treatment. RCC is highly heterogeneous, yet treatment guidelines rely predominantly on kidney renal [...] Read more.
Renal cell carcinoma (RCC) is the most common malignancy of the urinary system, characterized by high incidence, mortality, and resistance to therapy. Its molecular heterogeneity presents challenges for effective precision treatment. RCC is highly heterogeneous, yet treatment guidelines rely predominantly on kidney renal clear cell carcinoma (KIRC) studies, neglecting other molecular subtypes, which limits therapy personalization for non-KIRC patients. This study aimed to explore the role of small ubiquitin-like modifier (SUMOylation)-associated genes in the progression and prognosis of RCC and its subtypes. We identified 298 SUMOylation-associated differentially expressed genes (DEGs), including 151 RCC-specific genes after excluding expression changes attributable to RCC subtype-specific variation. Ten core genes (PRKCG, PRKCQ, PRKCD, IRS4, SLC2A4, SLC27A1, SLC27A4, LCN2, S100A7, and S100A9) were identified, with LCN2 expression not only discriminates tumor from normal tissue but also separates KIRC from KICH/KIRP, proposing LCN2 as a potential second-step biomarker for KIRC identification on top of traditional histology. Inter-subtype RCC heterogeneity represented a key factor limiting predictive performance of the six prognostic signature genes (CREB3L1, GNA11, PFKM, PPARGC1A, PPP2R2C and PRKCG). Its 5-year AUC exceeded 0.7 for every individual RCC subtype in the TCGA training cohort, with pooled 5-year AUCs of 0.61 (TCGA training cohort) and 0.67 (independent PCAWG validation cohort). The prognostic risk model demonstrated strong predictive performance, with a C-index of 0.791 before calibration and 0.774 after calibration. Importantly, the C-index remained above 0.75 throughout the 60-month follow-up period, indicating stable and robust long-term prognostic accuracy. High-risk patients exhibited greater immune cell infiltration, indicating potential for immunotherapy. Following secondary screening, three RCC cell lines (BFTC909, CAKI1, and CAL54) and five target genes (PRKCD, SLC27A1, SLC27A4, LCN2 and GNA11) were identified as optimal candidates for subsequent mechanistic investigations. This study uncovers the prognostic and functional relevance of SUMOylation in RCC and offers a novel framework for biomarker development, therapeutic targeting, and immunotherapeutic stratification. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Kidney Diseases)
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24 pages, 108617 KB  
Article
αB-Crystallin Protects Against Cisplatin-Induced Nephrotoxicity by Modulating Apoptosis In Vivo and In Vitro
by Sylia Ardache, Shu Tang and Endong Bao
Curr. Issues Mol. Biol. 2026, 48(7), 667; https://doi.org/10.3390/cimb48070667 - 29 Jun 2026
Viewed by 261
Abstract
Cisplatin (CP) chemotherapy is limited by nephrotoxicity, primarily involving tubular epithelial cell apoptosis. αB-crystallin (CryAB) is a small heat shock protein that plays a cytoprotective role in stressed kidneys but can also promote tumor progression. Its precise role and molecular mechanisms in CP-induced [...] Read more.
Cisplatin (CP) chemotherapy is limited by nephrotoxicity, primarily involving tubular epithelial cell apoptosis. αB-crystallin (CryAB) is a small heat shock protein that plays a cytoprotective role in stressed kidneys but can also promote tumor progression. Its precise role and molecular mechanisms in CP-induced kidney injury remain largely unclear. This study highlighted the function of CryAB and its regulatory pathways in CP nephrotoxicity by employing in vitro models of rat renal tubular epithelial cells (NRK-52E) with CryAB gene knockdown/overexpression, and in vivo models of CryAB knockout/wild-type mice, followed by CP treatment. Apoptosis and key signaling pathways (NF-κB, MAPK, AKT) were evaluated in this study. The results indicated that CP treatment (20 µM) significantly upregulated CryAB expression in renal cells (p < 0.01) and triggered both apoptosis and MAPK activation. CryAB deficiency sensitized cells and mice to CP, exacerbating renal dysfunction, tubular injury, and apoptosis, as evidenced by increased Bax, cyt c release, and caspase-3 cleavage. Conversely, CryAB overexpression attenuated these effects. Furthermore, our findings suggest that the lack of CryAB favors the cytoplasmic retention of NF-κB, and that CryAB status can influence MAPK signaling, pointing to a potential regulatory loop. Additionally, CP-induced AKT phosphorylation was diminished in CryAB-deficient models. Therefore, CryAB may exert a cytoprotective role in CP nephrotoxicity, potentially mitigating tubular apoptosis by modulating the mitochondrial apoptotic pathway, supporting NF-κB-mediated survival signaling, and cross-talking with MAPK and AKT pathways. Our findings suggest that CryAB serves as an important regulator of renal cell fate and a potential therapeutic target for mitigating CP-induced kidney injury. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Kidney Diseases)
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19 pages, 19917 KB  
Article
Lysimachia christinae Hance Extract Mitigates Kidney Stone Formation: Association with NOX2/ROS Axis Modulation and Ferroptosis
by Lian Xia, Zhaoguo Zhou, Chen Luo, Yan Yang, Daike Zou, Hanyue Zhang, Kaizhi Hu and Xianqin Luo
Curr. Issues Mol. Biol. 2026, 48(5), 520; https://doi.org/10.3390/cimb48050520 - 16 May 2026
Viewed by 1141
Abstract
Kidney stone disease is a common urinary system disorder with a continuously rising global incidence, posing a major public health challenge. As a classic traditional Chinese medicine for the treatment of kidney stones, Lysimachia christinae Hance (LCH) has not yet been fully elucidated [...] Read more.
Kidney stone disease is a common urinary system disorder with a continuously rising global incidence, posing a major public health challenge. As a classic traditional Chinese medicine for the treatment of kidney stones, Lysimachia christinae Hance (LCH) has not yet been fully elucidated in terms of its pharmacological mechanism. In this study, a rat model of calcium oxalate kidney stones and a calcium oxalate monohydrate (COM)-induced injury model of human renal tubular epithelial (HK-2) cells were established. Combined with transcriptomic analysis and experimental verification, the therapeutic effect and underlying molecular mechanism of LCH against kidney stones were systematically explored. Results demonstrated that LCH extract significantly reduced serum levels of blood urea nitrogen (BUN) and creatinine (Cr), as well as renal tissue levels of kidney injury molecule-1 (KIM-1) and cystatin-C (Cys-C) in rats with calcium oxalate crystal-induced renal injury, and diminished calcium oxalate crystal deposition and adhesion in rat renal tissues as well as HK-2 cells, thus exerting a robust renoprotective effect. Mechanistically, transcriptome sequencing indicated that the anti-nephrolithiasis effect of LCH was closely related to the inhibition of oxidative stress and ferroptosis. LCH extract reversed CaOx crystal-induced upregulation of NADPH oxidase 2 (NOX2) and downregulation of superoxide dismutase 2 (SOD2), reduced intracellular oxygen species (ROS) levels, downregulated the expression of transferrin receptor 1 (TFR1) and acyl-CoA synthetase long-chain family member 4 (ACSL4) while upregulating that of ferritin heavy chain 1 (FTH1), solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), and diminished intracellular iron accumulation, thereby effectively ameliorating crystal-mediated renal injury. The present study demonstrates that the therapeutic effect of LCH on kidney stones is closely related to the regulation of the NOX2/ROS signaling axis and ferroptosis, providing novel theoretical evidence for its clinical application. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Kidney Diseases)
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15 pages, 8399 KB  
Article
Magnolol Ameliorates Cisplatin-Induced Acute Kidney Injury with Activation of Nrf2-Associated Antioxidant Responses
by Mi-Gyeong Gwon, Min Hui Park and Jaechan Leem
Curr. Issues Mol. Biol. 2026, 48(1), 96; https://doi.org/10.3390/cimb48010096 - 17 Jan 2026
Cited by 1 | Viewed by 932
Abstract
Cisplatin (CDDP) is a cornerstone chemotherapeutic drug, yet its efficacy is frequently compromised by renal toxicity, primarily manifesting as acute kidney injury (AKI). Magnolol (MG) is a polyphenol from Magnolia officinalis and has been widely documented for its pronounced antioxidant and anti-inflammatory properties. [...] Read more.
Cisplatin (CDDP) is a cornerstone chemotherapeutic drug, yet its efficacy is frequently compromised by renal toxicity, primarily manifesting as acute kidney injury (AKI). Magnolol (MG) is a polyphenol from Magnolia officinalis and has been widely documented for its pronounced antioxidant and anti-inflammatory properties. This study evaluated the renoprotective effects of MG in a murine model of CDDP-induced AKI. Male C57BL/6 mice received MG (20 mg/kg) via daily intraperitoneal injection for four consecutive days, starting one day before a single CDDP injection. MG significantly reduced the serum concentrations of blood urea nitrogen and creatinine. Histopathological assessment revealed attenuated tubular damage and reduced expression of tubular injury markers. MG inhibited pro-inflammatory cytokines at both systemic and renal levels, alleviated endoplasmic reticulum stress, and suppressed activation of mitogen-activated protein kinase signaling pathways. Apoptotic damage was mitigated, as shown by the fewer TUNEL-positive cells and lowered expression of pro-apoptotic markers. In parallel, ferroptotic processes were alleviated through downregulation of pro-ferroptotic proteins and preservation of key antioxidant regulators. Importantly, MG restored nuclear factor erythroid 2-related factor 2 activity and upregulated downstream antioxidant effectors. These findings highlight the multi-targeted renoprotective actions of MG and support its possible utility as a therapeutic agent to prevent CDDP-induced renal injury. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Kidney Diseases)
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Review

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21 pages, 505 KB  
Review
Advances in the Treatment of Autosomal Dominant Polycystic Kidney Disease and Novel Therapeutic Targets
by Wenzheng Zhang, Tianze Sun, Xin Wang and Tao Jiang
Curr. Issues Mol. Biol. 2026, 48(5), 468; https://doi.org/10.3390/cimb48050468 - 30 Apr 2026
Viewed by 2796
Abstract
Autosomal dominant polycystic kidney disease (ADPKD), with a prevalence of approximately 1 in 1000, is the most common inherited cause of end-stage renal disease (ESRD). It is primarily caused by mutations in the PKD1 or PKD2 genes. Multiple studies have demonstrated that deficiency [...] Read more.
Autosomal dominant polycystic kidney disease (ADPKD), with a prevalence of approximately 1 in 1000, is the most common inherited cause of end-stage renal disease (ESRD). It is primarily caused by mutations in the PKD1 or PKD2 genes. Multiple studies have demonstrated that deficiency of polycystin proteins, dysregulation of signaling pathways, and activation of inflammatory factors contribute to the progression of ADPKD. The cAMP-targeting drug tolvaptan is currently the only approved therapy for ADPKD; however, its side effects and high cost have limited its widespread use. Meanwhile, mTOR inhibitors, AMPK-targeting agents, anti-inflammatory agents, and dietary interventions have shown promising results in treating ADPKD. Furthermore, the emergence of novel targets such as Notch3 and AURKA offers new directions for ADPKD therapy. This article aims to review the pathogenesis of ADPKD and current treatment advances, while exploring potential new targets for future research, hoping to provide a scientific theoretical foundation for disease management. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Kidney Diseases)
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