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Cells
Special Issues
Acute Kidney Injury: From Molecular Mechanisms to Diseases
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Acute Kidney Injury: From Molecular Mechanisms to Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1500

Special Issue Editors

Prof. Dr. Zheng Dong

E-Mail Website
Guest Editor
Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University, R&E Building, CB1124, Augusta, GA, USA
Interests: cell death; kidney injury regeneration; kidney repair; mitochondria; metabolism; autophagy; epigenetic regulation
Prof. Dr. Hassan Dihazi

E-Mail Website1 Website2
Guest Editor
1. Department of Nephrology and Rheumatology, Göttingen University Medical Center, Georg August University, Göttingen, Germany
2. Centre for Biostructural Imaging of Neurodegeneration (BIN), University Medical Center Göttingen, Georg August University, Göttingen, Germany
Interests: understanding the pathomechanisms of kidney diseases; investigating therapeutic targets for kidney fibrosis; ER stress proteins and UPR in kidney fibrosis; biomarker discovery and validation
Special Issues, Collections and Topics in MDPI journals
Dr. Huihui Huang

E-Mail Website
Guest Editor
Harvard Medical School, Boston, MA, USA
Interests: mitochondrial biogenesis; metabolites; acute kidney injury; chronic kidney disease

Special Issue Information

Dear Colleagues,

The kidney requires  substantial adenosine triphosphate to remove waste from the blood and regulate fluid and electrolyte balance. Aberrations in energy flow can lead to cellular dysfunction and death. Mitochondria provide the energy to drive these essential functions. Mitochondrial dysfunction leads to the development of acute kidney injury and failure of recovery. Pathways of energy metabolism and mitochondrial dysfunction are emerging as critical drivers of acute kidney injury and represent new potential targets for treatment. Multiple novel regulators or metabolites such as PGC-1alpha, QPRT, NAD+ have been discovered in decades  and some mitochondrial-targeted antioxidants including SS-31 and CoQ10 are under clinic trials.

We invite all scientists working in the acute kidney injury field to participate in this Special Issue. Original research articles, reviews, or shorter perspective articles on all aspects related to acute kidney injury are welcome, including topics such as new molecular and cellular functions of the key players in acute kidney injury including but not limited to mitochondrial dysfunction, energy utilization, changes in metabolism and regulated cell death, and novel approaches with current, under clinical development, or newly emerging inhibitors which target to acute kidney injury.

Prof. Dr. Zheng Dong
Prof. Dr. Hassan Dihazi
Dr. Huihui Huang
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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
  • mitochondrial dysfunction
  • signal pathways
  • metabolites

Published Papers (1 paper)

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Research

26 pages, 5503 KiB  
Article
The Protective Pathways Activated in Kidneys of αMUPA Transgenic Mice Following Ischemia\Reperfusion-Induced Acute Kidney Injury
by Heba Abd Alkhaleq, Tony Karram, Ahmad Fokra, Shadi Hamoud, Aviva Kabala and Zaid Abassi
Cells 2023, 12(20), 2497; https://doi.org/10.3390/cells12202497 - 20 Oct 2023
Cited by 1 | Viewed by 1037
Abstract
Despite the high prevalence of acute kidney injury (AKI), the therapeutic approaches for AKI are disappointing. This deficiency stems from the poor understanding of the pathogenesis of AKI. Recent studies demonstrate that αMUPA, alpha murine urokinase-type plasminogen activator (uPA) transgenic mice, display a [...] Read more.
Despite the high prevalence of acute kidney injury (AKI), the therapeutic approaches for AKI are disappointing. This deficiency stems from the poor understanding of the pathogenesis of AKI. Recent studies demonstrate that αMUPA, alpha murine urokinase-type plasminogen activator (uPA) transgenic mice, display a cardioprotective pathway following myocardial ischemia. We hypothesize that these mice also possess protective renal pathways. Male and female αMUPA mice and their wild type were subjected to 30 min of bilateral ischemic AKI. Blood samples and kidneys were harvested 48 h following AKI for biomarkers of kidney function, renal injury, inflammatory response, and intracellular pathways sensing or responding to AKI. αMUPA mice, especially females, exhibited attenuated renal damage in response to AKI, as was evident from lower SCr and BUN, normal renal histology, and attenuated expression of NGAL and KIM-1. Notably, αMUPA females did not show a significant change in renal inflammatory and fibrotic markers following AKI as compared with wild-type (WT) mice and αMUPA males. Moreover, αMUPA female mice exhibited the lowest levels of renal apoptotic and autophagy markers during normal conditions and following AKI. αMUPA mice, especially the females, showed remarkable expression of PGC1α and eNOS following AKI. Furthermore, MUPA mice showed a significant elevation in renal leptin expression before and following AKI. Pretreatment of αMUPA with leptin-neutralizing antibodies prior to AKI abolished their resistance to AKI. Collectively, the kidneys of αMUPA mice, especially those of females, are less susceptible to ischemic I/R injury compared to WT mice, and this is due to nephroprotective actions mediated by the upregulation of leptin, eNOS, ACE2, and PGC1α along with impaired inflammatory, fibrotic, and autophagy processes. Full article
(This article belongs to the Special Issue Acute Kidney Injury: From Molecular Mechanisms to Diseases)
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