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Biomedicines
Special Issues
Kidney Injury/Failure: Molecular Mechanisms and Clues for Intervention
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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: 30 June 2025 | Viewed by 5814

Special Issue Editor

Dr. Chang Chu

E-Mail Website
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

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. Biomedicines 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 2600 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.

Keywords

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

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Published Papers (3 papers)

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Research

14 pages, 1561 KiB  
Article
Chrysin Attenuates Gentamicin-Induced Renal Injury in Rats Through Modulation of Oxidative Damage and Inflammation via Regulation of Nrf2/AKT and NF-kB/KIM-1 Pathways
by Talat A. Albukhari, Rehab M. Bagadood, Bayan T. Bokhari, Waheed A. Filimban, Hatem Sembawa, Nani Nasreldin, Hossam E. Gadalla and Mohamed E. El-Boshy
Biomedicines 2025, 13(2), 271; https://doi.org/10.3390/biomedicines13020271 - 23 Jan 2025
Cited by 1 | Viewed by 1121
Abstract
Background: Gentamicin (GM) is extensively used as an antibiotic for the treatment of infections caused by Gram-negative bacteria. Oxidative stress and proinflammatory cytokines are implicated in GM-induced renal damage. Chrysin (CH), also known as 5,7-dihydroxyflavone, has been used in traditional medicine to treat [...] Read more.
Background: Gentamicin (GM) is extensively used as an antibiotic for the treatment of infections caused by Gram-negative bacteria. Oxidative stress and proinflammatory cytokines are implicated in GM-induced renal damage. Chrysin (CH), also known as 5,7-dihydroxyflavone, has been used in traditional medicine to treat various kidney disorders. The aim of this study was to investigate the antioxidant, anti-apoptotic, and anti-inflammatory effects of CH against nephrotoxicity induced by GM. Methods: Male rats were separated into four equal groups: a negative control group (NC), a CH-treated group (100 mg/kg/day per os), a group treated with GM (100 mg/kg/day IM), and a group treated with both GM and CH (100 mg/kg/day), for 10 days. Blood and urine renal markers were investigated. Results: GM caused increases in the serum creatinine and urea levels and decreases in creatinine clearance, urine flow, and urine volume in the GM-treated rats. Moreover, there were increases in the levels of IL-1β, TNF-α, IL-18, and MDA in the renal tissues, with an augmented expression of NF-κB/KIM-1, as well as decreases in antioxidant marker (GSH, GPx, CAT, and SOD) activities and decreased expressions of the anti-inflammatory transcription factors Nrf2 and AKT. The simultaneous treatment with CH in the GM-treated group protected renal tissues against the nephrotoxicity induced by GM, as demonstrated by the normalization of renal markers and improvement in histopathological damage. Conclusions: This study reveals that CH may attenuate GM-induced renal toxicity in rats. Full article
(This article belongs to the Special Issue Kidney Injury/Failure: Molecular Mechanisms and Clues for Intervention)
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21 pages, 4439 KiB  
Article
Potential Nephroprotective Effect of uPA against Ischemia/Reperfusion-Induced Acute Kidney Injury in αMUPA Mice and HEK-293 Cells
by Heba Abd Alkhaleq, Israel Hacker, Tony Karram, Shadi Hamoud, Aviva Kabala and Zaid Abassi
Biomedicines 2024, 12(10), 2323; https://doi.org/10.3390/biomedicines12102323 - 12 Oct 2024
Viewed by 1236
Abstract
Background/Objectives: The incidence of acute kidney injury (AKI) has been steadily increasing. Despite its high prevalence, there is no pathogenetically rational therapy for AKI. This deficiency stems from the poor understanding of the pathogenesis of AKI. Renal ischemia/hypoxia is one of the leading [...] Read more.
Background/Objectives: The incidence of acute kidney injury (AKI) has been steadily increasing. Despite its high prevalence, there is no pathogenetically rational therapy for AKI. This deficiency stems from the poor understanding of the pathogenesis of AKI. Renal ischemia/hypoxia is one of the leading causes of clinical AKI. This study investigates whether αMUPA mice, overexpressing the urokinase plasminogen activator (uPA) gene are protected against ischemic AKI, thus unraveling a potential renal damage treatment target. Methods: We utilized an in vivo model of I/R-induced AKI in αMUPA mice and in vitro experiments of uPA-treated HEK-293 cells. We evaluated renal injury markers, histological changes, mRNA expression of inflammatory, apoptotic, and autophagy markers, as compared with wild-type animals. Results: the αMUPA mice exhibited less renal injury post-AKI, as was evident by lower SCr, BUN, and renal NGAL and KIM-1 along attenuated adverse histological alterations. Notably, the αMUPA mice exhibited decreased levels pro-inflammatory, fibrotic, apoptotic, and autophagy markers like TGF-β, IL-6, STAT3, IKB, MAPK, Caspase-3, and LC3. By contrast, ACE-2, p-eNOS, and PGC1α were higher in the kidneys of the αMUPA mice. In vitro results of the uPA-treated HEK-293 cells mirrored the in vivo findings. Conclusions: These results indicate that uPA modulates key pathways involved in AKI, offering potential therapeutic targets for mitigating renal damage. Full article
(This article belongs to the Special Issue Kidney Injury/Failure: Molecular Mechanisms and Clues for Intervention)
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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 12 | Viewed by 2630
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
(This article belongs to the Special Issue Kidney Injury/Failure: Molecular Mechanisms and Clues for Intervention)
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