Kidney Injury/Failure: Molecular Mechanisms and Clues for Intervention

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 1779

Special Issue Editor


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Guest Editor
1. Fifth Department of Medicine (Nephrology/Endocrinology/Rheumatology), University Medical Centre Mannheim, University of Heidelberg, 68167 Mannheim, Germany
2. Department of Nephrology, Charite University Berlin, 13353 Berlin, Germany
Interests: acute kidney injury; chronic kidney disease; dialysis; sodium–glucose cotransporter 2 inhibitors; angiogenesis biomarkers

Special Issue Information

Dear Colleagues,

Kidney injury/failure is a significant health concern worldwide and has been classified into two syndromes—acute kidney injury (AKI) and chronic kidney disease (CKD). However, a close interconnection between these two syndromes has recently been found. These two syndromes are independent risk factors for each other, and they are both risk factors for cardiovascular disease, resulting in greater mortality in patients with kidney failure. Currently, therapeutic approaches for patients with AKI and/or early-stage CKD include the prevention of nephrotoxic substances, lifestyle modifications, supportive care, Renin–angiotensin–aldosterone system (RAAS) inhibitors, and comorbidities management, but interventions for pathophysiological changes in the kidney itself remain limited. New therapeutic approaches are therefore needed to slow the deterioration of kidney function and even halt kidney impairment through early intervention. Therefore, this Special Issue aims to explore the latest advancements in understanding the complicated molecular and cellular pathways, and novel treatments of kidney injury. It provides a platform for researchers to share their insights and contribute to improving patient outcomes in kidney injury/failure with topics including but not limited to:

  1. Cellular and molecular pathways involved in kidney injury.
  2. Oxidative stress, inflammation, and immune responses in acute kidney injury or chronic kidney failure.
  3. Clinical trials/observational studies investigating novel treatments and interventions for kidney injury.
  4. Basic experiment of new therapeutic strategies for kidney injury.

Dr. Chang Chu
Guest Editor

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Keywords

  • acute kidney injury
  • chronic kidney diseases
  • molecular mechanisms
  • cellular mechanisms
  • new interventions
  • therapeutic approaches

Published Papers (1 paper)

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Research

17 pages, 9734 KiB  
Article
YAP/ACSL4 Pathway-Mediated Ferroptosis Promotes Renal Fibrosis in the Presence of Kidney Stones
by Lei Li, Zehua Ye, Yuqi Xia, Bojun Li, Lijia Chen, Xinzhou Yan, Tianhui Yuan, Baofeng Song, Weimin Yu, Ting Rao, Fangyou Lin, Xiangjun Zhou and Fan Cheng
Biomedicines 2023, 11(10), 2692; https://doi.org/10.3390/biomedicines11102692 - 1 Oct 2023
Cited by 2 | Viewed by 1419
Abstract
The potential association between calcium oxalate stones and renal fibrosis has been extensively investigated; however, the underlying mechanisms remain unclear. Ferroptosis is a novel form of cell death characterized by iron-dependent lipid peroxidation and regulated by acyl coenzyme A synthase long-chain family member [...] Read more.
The potential association between calcium oxalate stones and renal fibrosis has been extensively investigated; however, the underlying mechanisms remain unclear. Ferroptosis is a novel form of cell death characterized by iron-dependent lipid peroxidation and regulated by acyl coenzyme A synthase long-chain family member 4 (ACSL4). Yes-associated protein (YAP), a transcriptional co-activator in the Hippo pathway, promotes ferroptosis by modulating ACSL4 expression. Nevertheless, the involvement of YAP–ACSL4 axis-mediated ferroptosis in calcium oxalate crystal deposition-induced renal fibrosis and its molecular mechanisms have not been elucidated. In this study, we investigated ACSL4 expression and ferroptosis activation in the kidney tissues of patients with calcium oxalate stones and in mice using single-cell sequencing, transcriptome RNA sequencing, immunohistochemical analysis, and Western blot analysis. In vivo and in vitro experiments demonstrated that inhibiting ferroptosis or ACSL4 mitigated calcium oxalate crystal-induced renal fibrosis. Furthermore, YAP expression was elevated in the kidney tissues of patients with calcium oxalate stones and in calcium oxalate crystal-stimulated human renal tubular epithelial cell lines. Mechanistically, in calcium oxalate crystal-stimulated human renal tubular epithelial cell lines, activated YAP translocated to the nucleus and enhanced ACSL4 expression, consequently inducing cellular ferroptosis. Moreover, YAP silencing suppressed ferroptosis by downregulating ACSL4 expression, thereby attenuating calcium oxalate crystal-induced renal fibrosis. Conclusively, our findings suggest that YAP–ACSL4-mediated ferroptosis represents an important mechanism underlying the induction of renal fibrosis by calcium oxalate crystal deposition. Targeting the YAP–ACSL4 axis and ferroptosis may therefore hold promise as a potential therapeutic approach for preventing renal fibrosis in patients with kidney stones. Full article
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