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Molecular Mechanisms in Kidney Disease

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 July 2025) | Viewed by 715

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Special Issue Information

Dear Colleagues,

The kidneys play a vital role in maintaining overall health by regulating the excretion of waste products, salts, and water and performing several essential physiological functions. These include waste removal, reabsorption of critical nutrients, acid-base balance, electrolyte and water homeostasis, and hormone production. However, when kidney function declines to less than 15% due to acute or chronic insults, it can lead to a cascade of severe health complications, such as coagulation disorders, cardiovascular dysfunction, vascular calcification, cancer, and cognitive impairments. Persistent unresolved damage following acute or chronic kidney injury often results in maladaptive repair processes, which accelerate renal fibrosis. This progression is driven by disruptions in redox homeostasis, heightened inflammatory responses, and the senescence or death of renal tubular cells. Despite advances in nephrology, the cellular and molecular mechanisms underpinning the pathology of kidney diseases remain incompletely understood. Current treatments for kidney diseases are suboptimal, underscoring the urgent need to elucidate the mechanisms driving these conditions. A deeper understanding of these molecular and cellular pathways can pave the way for innovative therapeutic strategies to prevent and treat kidney diseases more effectively. To advance this goal, we invite researchers to contribute to the Special Issue titled "Molecular Mechanisms in Kidney Disease". This collection seeks to bring together original research articles and comprehensive reviews addressing the diverse aspects of kidney diseases. By fostering a platform for cutting-edge research, this Special Issue aspires to advance our understanding of kidney injury and repair mechanisms, ultimately improving patient outcomes.

Prof. Dr. Tzong-Shyuan Lee
Guest Editor

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Keywords

  • kidney disease
  • inflammation
  • redox
  • senescence
  • cell death
  • fibrosis
  • signaling pathway
  • uremic syndrome
  • cardiorenal syndrome
  • gut–kidney axis

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Published Papers (1 paper)

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Research

21 pages, 18076 KiB  
Article
Oxidized Albumin Induces Renal Tubular Cell Death and Promotes the Progression of Renal Diseases Through Ferroptosis
by Yingyu Zhang, Rui Jiang, Zhuheng Shi, Yang Sui, Jie Cheng, Mika Suda, Manabu Niimi, Kun Gao, Jianglin Fan and Jian Yao
Int. J. Mol. Sci. 2025, 26(13), 5924; https://doi.org/10.3390/ijms26135924 - 20 Jun 2025
Viewed by 415
Abstract
Oxidative stress plays a crucial role in disease pathogenesis. While reactive oxygen species (ROS) directly cause cellular injury, emerging evidence suggests oxidatively modified proteins like albumin may also contribute significantly to tissue damage. Although oxidized albumin (ox-Alb) is linked to renal pathology, the [...] Read more.
Oxidative stress plays a crucial role in disease pathogenesis. While reactive oxygen species (ROS) directly cause cellular injury, emerging evidence suggests oxidatively modified proteins like albumin may also contribute significantly to tissue damage. Although oxidized albumin (ox-Alb) is linked to renal pathology, the direct effects and mechanisms of ox-Alb on renal cell injury remain unclear. This study was created to address these questions. In mouse models of renal injury initiated by vitamin C/copper or ischemia/reperfusion, levels of serum ox-Alb were significantly elevated. The treatment of albumin with copper/vitamin C increased Alb carbonylation and reduced the number of sulfhydryl groups, causing Alb oxidation. In cultured renal tubular epithelial NRK-52E cells, ox-Alb triggered cell death, associated with increased intracellular albumin accumulation—enhanced cellular protein carbonylation, and p38 MAPK activation. Notably, ox-Alb induced ferroptosis, evidenced by decreased GPX4 and xCT, increased ACSL4, elevated iron and lipid peroxidation, and suppression by deferoxamine and liproxstatin-1. In vivo, administration of ox-Alb exacerbated doxorubicin-induced nephropathy, as indicated by the elevated BUN, creatinine, and proteinuria, and intensified renal ferroptotic responses, including altered GPX4 and ACSL4. Our findings demonstrate that ox-Alb induces renal cell ferroptosis and promotes renal disease progression, suggesting its pivotal pathogenic role in oxidative stress-related kidney diseases. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Kidney Disease)
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