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Recent Advances in Molecular Mechanisms Underlying Kidney Diseases: Pathophysiology and Therapeutic Targets, 2nd Edition

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: 20 July 2025 | Viewed by 6613

Special Issue Editor

Dr. George J. Dugbartey

E-Mail Website
Guest Editor
Department of Surgery, London Health Sciences Center, University of Western Ontario, London, ON N6A 5C1, Canada
Interests: kidney diseases; pharmacotherapy; kidney transplantation; cellular and molecular mechanisms; renal protection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Kidney diseases remain a major public health concern associated with the increasing morbidity and mortality of millions of people globally. Unfortunately, the prevalence of kidney diseases has increased significantly in recent times. The hallmarks of this important human pathology include the excessive accumulation and deposition of extracellular matrix, mesangiolysis, glomerular basement membrane thickening, tubulointerstitial fibrosis and many more, which eventually lead to loss of kidney function. As the pathogenesis of different forms of kidney diseases is multifactorial, several experimental models have recently been developed to mimic clinical situations and provide a mechanistic understanding of the various pathologies of kidney diseases, with the ultimate goal of identifying and developing potential therapeutic targets. These experimental models have identified several molecular mechanisms underlying various forms of kidney diseases. These mechanisms include:

  • PI3K/Akt/mTOR pathway;
  • Jak/Stat and inflammatory signaling pathways;
  • Induction of oxidative stress and apoptotic pathways;
  • Upregulation of renal transforming growth factor beta-1 expression;
  • Activation of fibroblast and renin-angiotensin-aldosterone system;
  • Mitochondrial dysfunction and depletion of adenosine triphosphate.

Targeting various molecular mechanisms underlying the pathophysiology of the different forms of kidney diseases has shown to be beneficial, and offers a huge potential to be explored that is amenable to novel therapies. This Special Issue focuses on recent research developments in the pathophysiology of kidney diseases and their therapeutic targets for diagnosis and treatment.

Original papers, review articles, and perspectives from experts in the field are welcome.

Dr. George J. Dugbartey
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 diseases
  • pathophysiology
  • molecular mechanisms
  • therapeutic targets
  • acute kidney injury
  • chronic kidney disease
  • polycystic kidney disease
  • end-stage renal disease
  • IgA nephropathy
  • diabetic nephropathy
  • hypertensive nephropathy
  • renal cancer
  • kidney infarction
  • kidney infection
  • kidney failure
  • kidney stones
  • renal tubular acidosis
  • renal artery stenosis
  • acute tubular necrosis
  • glomerulopathy
  • interstitial nephritis
  • nephrotic syndrome
  • simple kidney cyst

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Published Papers (4 papers)

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Research

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15 pages, 6322 KiB  
Article
Gender Differences in Adenine Diet-Induced Kidney Toxicity: The Impact of 17β-Estradiol on Renal Inflammation and Fibrosis
by Sugyeong Ha, Minjung Son, Jeongwon Kim, Doyeon Kim, Mi-Jeong Kim, Jian Yoo, Byeong Moo Kim, Donghwan Kim, Hae Young Chung and Ki Wung Chung
Int. J. Mol. Sci. 2025, 26(3), 1358; https://doi.org/10.3390/ijms26031358 - 6 Feb 2025
Viewed by 829
Abstract
Chronic kidney disease (CKD) involves ongoing impairment of kidney function and structural changes. Previous studies indicated that males have a substantially higher prevalence of CKD than those observed in females. Here, we compared the gender differences in CKD development by comparing age-matched male [...] Read more.
Chronic kidney disease (CKD) involves ongoing impairment of kidney function and structural changes. Previous studies indicated that males have a substantially higher prevalence of CKD than those observed in females. Here, we compared the gender differences in CKD development by comparing age-matched male and female mice subjected to a 0.25% adenine diet (AD) for two weeks. Male mice showed a significantly greater decrease in kidney function than female mice, as evidenced by the elevated blood urea nitrogen levels (M-AD: 160 ± 5 mg/dL, F-AD: 90 ± 4 mg/dL; p < 0.001). Furthermore, male mice kidneys exhibited pronounced tubule dilation and kidney damage, as detected by histological and biochemical methods. The extent of fibrosis was quantified using multiple biological methods, revealing a greater degree of fibrosis in male kidneys. We next indicated the inflammatory responses in the kidneys. Similar to the extent of fibrosis, AD-fed male mice showed significantly increased levels of pro-inflammatory markers, including cytokine expression and infiltration of immune cell, compared to female mice. Based on in vivo observations, the anti-inflammatory and anti-fibrotic effects of 17β-estradiol (E2) were further evaluated in vitro conditions. E2 pre-treatment significantly reduced lipopolysaccharide-induced inflammatory response through inhibition of the nuclear factor-kappa B (NF-κB) pathway in NRK52E renal epithelial cells. In NRK49F renal fibroblasts, E2 pre-treatment also reduced TGFβ-induced fibrotic responses. We further demonstrated that E2 markedly decreased fibrosis and inflammation in AD-fed mouse kidneys. Our observations revealed that male mice kidneys exhibited a heightened inflammatory and fibrotic response compared to female mice kidneys. Additionally, our findings suggest that the observed sex differences may be partially attributed to the potential anti-inflammatory and anti-fibrotic effects of E2. Full article
(This article belongs to the Special Issue Recent Advances in Molecular Mechanisms Underlying Kidney Diseases: Pathophysiology and Therapeutic Targets, 2nd Edition)
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20 pages, 5057 KiB  
Article
Chemoprotective Mechanism of Sodium Thiosulfate Against Cisplatin-Induced Nephrotoxicity Is via Renal Hydrogen Sulfide, Arginine/cAMP and NO/cGMP Signaling Pathways
by George J. Dugbartey, Karl K. Alornyo, Ismaila Adams, Samuel Adjei, Daniel Amoah and Richard Obeng-Kyeremeh
Int. J. Mol. Sci. 2025, 26(1), 384; https://doi.org/10.3390/ijms26010384 - 4 Jan 2025
Viewed by 3257
Abstract
Cisplatin is a common and highly effective chemotherapeutic agent whose nephrotoxic side effect is well-characterized. Sodium thiosulfate (STS), an FDA-approved hydrogen sulfide (H2S) donor drug, is emerging as a chemoprotective agent against cisplatin-induced nephrotoxicity (CIN). In this study, we investigated the [...] Read more.
Cisplatin is a common and highly effective chemotherapeutic agent whose nephrotoxic side effect is well-characterized. Sodium thiosulfate (STS), an FDA-approved hydrogen sulfide (H2S) donor drug, is emerging as a chemoprotective agent against cisplatin-induced nephrotoxicity (CIN). In this study, we investigated the chemoprotective mechanism of STS in a rat model of CIN. Twenty-five male Sprague Dawley rats were randomly assigned to the following groups: HC: Healthy control (received 10 mL/kg/day of 0.9% saline intraperitoneally (ip), [n = 5]), CIN: Cisplatin (received single dose of 7 mg/kg cisplatin ip [n = 5]); CIN + PAG: Cisplatin and daily ip administration of 40 mg/kg of the H2S inhibitor, DL-propargylglycine (PAG) for 28 days (n = 5); CIN + PAG + STS: Cisplatin and daily PAG and STS (150 µM) ip injection for 28 days; CIN + STS: Cisplatin and daily STS ip administration for 28 days (n = 5). Rats in each group were kept in metabolic cages for 24 h on day 0, 14 and 29 after cisplatin administration for urine collection. Rats were then euthanized, and kidney and blood samples were collected for analysis. Histologically, CIN was characterized by glomerular and tubular injury and significant macrophage influx and tubular apoptosis, as well as markedly increased levels of plasma and renal IL-1β, IL-6 and TNF-α and impaired renal antioxidant status compared to HC rats (p < 0.001). These pathological changes were exacerbated in CIN + PAG rats and were strongly reduced in CIN + PAG + STS rats relative to CIN + PAG rats (p < 0.01), while superior renal protection was observed in CIN + STS rats. Functionally, CIN was evidenced by markedly increased levels of serum creatinine and BUN, and significantly decreased urine creatinine, renal creatinine clearance, as well as electrolyte imbalance and urinary concentrating defect in comparison with HC (p < 0.01). These functional changes worsened significantly in CIN + PAG rats (p < 0.05) but improved in CIN + PAG + STS rats, with further improvement in CIN + STS rats to levels comparable to HC rats. Mechanistically, STS increased renal and plasma levels of H2S, arginine, cAMP, nitric oxide (NO) and cGMP as well as SIRT3 and PGC-1α. We have shown for the first time that STS provides chemoprotection against CIN by activating renal arginine/cAMP and NO/cGMP signaling pathways and their downstream mechanisms through increased renal H2S production. Full article
(This article belongs to the Special Issue Recent Advances in Molecular Mechanisms Underlying Kidney Diseases: Pathophysiology and Therapeutic Targets, 2nd Edition)
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Review

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14 pages, 916 KiB  
Review
The Crosstalk Between NETs and the Complement Cascade: An Overview in Nephrological Autoimmune Disease
by Xhuliana Kajana, Gianluca Caridi, Maurizio Bruschi, Sonia Spinelli, Francesca Lugani, Gian Marco Ghiggeri, Edoardo La Porta, Gabriele Mortari, Enrico E. Verrina, Andrea Angeletti and Carolina Bigatti
Int. J. Mol. Sci. 2025, 26(6), 2789; https://doi.org/10.3390/ijms26062789 - 20 Mar 2025
Viewed by 460
Abstract
The complement cascade and Neutrophil Extracellular Traps (NETs) represent fundamental tools in protecting the host from foreign pathogens. Complement components and relative fragments, classically assigned to the innate immunity, represent a key link with the humoral immune response. NETs are a crucial component [...] Read more.
The complement cascade and Neutrophil Extracellular Traps (NETs) represent fundamental tools in protecting the host from foreign pathogens. Complement components and relative fragments, classically assigned to the innate immunity, represent a key link with the humoral immune response. NETs are a crucial component of the innate immune response, consisting of chromatin release from activated neutrophils. These web-like structures facilitate pathogen entrapment and elimination through proteolytic degradation and antimicrobial effectors. Previous findings suggested complement components and NETs have a significant role in the pathogenesis of several diseases characterized by inflammation, such as autoimmune and infectious diseases. However, the crosstalk between NETs and the complement cascade has only recently been investigated, and several aspects still need to be fully clarified. Recent evidence seems to suggest a bidirectional link between the complement cascade and NETosis. We here present the interaction between complement components and NETs in specific autoimmune diseases that mostly affect the kidney, such as systemic lupus erythematosus, Antineutrophilic Cytoplasmic Antibody (ANCA)-associated vasculitis and antiphospholipid syndrome. The mechanisms reported here may represent specific targets for the development of possible therapeutic strategies. Full article
(This article belongs to the Special Issue Recent Advances in Molecular Mechanisms Underlying Kidney Diseases: Pathophysiology and Therapeutic Targets, 2nd Edition)
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18 pages, 669 KiB  
Review
Exploring the Efficacy and Safety of Ketamine for Managing Acute Renal Colic in Emergency Departments: A Systematic Review of Recent Clinical Trials
by Shiryn D. Sukhram, Grozdena Yilmaz, Stephanie Erichsen and Sergey Vassilevich
Int. J. Mol. Sci. 2025, 26(1), 371; https://doi.org/10.3390/ijms26010371 - 4 Jan 2025
Viewed by 1377
Abstract
Kidney stones typically present as renal colic in emergency departments (EDs), where patients experience severe pain and often require parenteral therapy for symptom management. The economic burden associated with managing kidney stones exceeds USD 5 billion annually in the US and accounts for [...] Read more.
Kidney stones typically present as renal colic in emergency departments (EDs), where patients experience severe pain and often require parenteral therapy for symptom management. The economic burden associated with managing kidney stones exceeds USD 5 billion annually in the US and accounts for more than a million visits to EDs each year. There is clear evidence emphasizing the need for innovative and alternative pain control options for patients with renal colic. Recent randomized controlled trials suggest that intranasal (IN) and intravenous (IV) ketamine are as effective as parenteral NSAIDs and opioids in treating renal colic. However, the limited studies available show inconsistent results regarding the analgesic effects of ketamine. In this study, we reviewed the mechanism of action of ketamine for kidney stones, its efficacy in treating acute renal colic, and the potential adverse side effects of ketamine treatment. A population, intervention, comparison, and outcome (PICO)-related question was formulated to guide our research inquiry: “What are the effects of IV or IN ketamine, as a single agent or as an adjuvant (I), in adult patients diagnosed with acute renal colic (P) on pain scale scores and adverse side effects (O) compared to NSAIDs and/or opioids (C)?” Full article
(This article belongs to the Special Issue Recent Advances in Molecular Mechanisms Underlying Kidney Diseases: Pathophysiology and Therapeutic Targets, 2nd Edition)
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