Molecular Mechanisms of Kidney Injury and Repair II

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (15 October 2023) | Viewed by 1726

Special Issue Editor


E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AK, USA
Interests: ischemia- and toxicant-induced acute kidney injury; bioenergetics; mitochondrial dysfunction; protein phosphorylation; proteomics; protein kinases; cell injury; mechanisms of cell death
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Kidney disease remains a global public health concern because of high morbidity and mortality, and the significant healthcare costs associated with this disease. Chronic kidney disease gradually leads to a reduced quality of life. Ischemia, hypoxia, exposure to nephrotoxic compounds, and infections are the leading causes of acute kidney injury, which is encountered in a variety of clinical settings and is characterized by a rapid decline in kidney function and the failure to regulate fluids, electrolytes, and the acid–base balance. Evidence collected over the past 2 years suggests that SARS-CoV-2 infection may result in acute kidney injury followed by renal fibrosis. The mechanisms of renal injury caused by SARS-CoV-2 infection are not fully elucidated and could include the direct infection of the kidneys, or indirect mechanisms such as endothelial cell injury, thrombus formation, hypoxia, and changes in the oxidative metabolism of fuels. The signaling pathway originating from ACE2 may play a major role in mediating the acute renal injury caused by SARS-CoV-2.

The pathogenesis of acute kidney injury is associated with a series of cellular responses to the initial insult that involve different pathways and mechanisms, and a large variety of molecular targets. If the injury and stress are not too severe, repair processes are activated to replace lost cells, restore cellular metabolism and functions, and recover kidney functions. If the insult is prolonged or too severe, cellular stress and tissue dysfunction continue and the inflammatory cells are recruited to the kidney, initiating events that lead to inflammation, fibrosis, and eventually the progressive loss of renal function characteristic of chronic kidney disease. Progress made in understanding these complex mechanisms has resulted in the development of new biomarkers to diagnose acute kidney injury and its progression to chronic kidney disease.

Given the success of the first edition, we believe it is time to launch the second edition of this Special Issue. This Special Issue of Biomolecules seeks manuscripts that 1) identify molecular targets that are involved in mediating renal cell injury and/or promoting the repair of these cells after injury; 2) elucidate cellular, subcellular, and molecular mechanisms and pathways mediating kidney repair and recovery; and 3) propose therapeutic interventions to diminish or treat kidney injury or promote kidney recovery. In particular, we would like to encourage the submission of manuscripts that highlight the most recent findings regarding the mechanisms of acute kidney injury caused by SARS-CoV-2 infection and renal complications associated with this infection. We encourage scientists working in this area of research to submit original research articles, communications, and/or critical reviews that synthesize the current literature and discuss emerging directions in this field.

Prof. Dr. Grazyna Nowak
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. Biomolecules 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 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

  • pathogenesis of acute and chronic kidney injury
  • ischemic and/or nephrotoxic kidney injury
  • SARS-CoV2-induced kidney injury
  • glomerular/interstitial/vascular damage
  • different mechanisms of tubular cell death
  • inflammatory signals and fibrosis
  • bioenergetics, mitochondrial damage and biogenesis
  • autophagy and mitophagy
  • receptors and signaling pathways involved in kidney injury
  • cell cycle proteins
  • biomarkers
  • renal repair and regeneration
  • cytoprotection and therapeutic intervention
  • in vivo and in vitro models of kidney injury

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

14 pages, 1299 KiB  
Review
MicroRNA193a: An Emerging Mediator of Glomerular Diseases
by Joyita Bharati, Megan Kumar, Neil Kumar, Ashwani Malhotra and Pravin C. Singhal
Biomolecules 2023, 13(12), 1743; https://0-doi-org.brum.beds.ac.uk/10.3390/biom13121743 - 04 Dec 2023
Viewed by 1363
Abstract
MicroRNAs (miRNAs) are noncoding small RNAs that regulate the protein expression of coding messenger RNAs. They are used as biomarkers to aid in diagnosing, prognosticating, and surveillance of diseases, especially solid cancers. MiR-193a was shown to be directly pathogenic in an experimental mouse [...] Read more.
MicroRNAs (miRNAs) are noncoding small RNAs that regulate the protein expression of coding messenger RNAs. They are used as biomarkers to aid in diagnosing, prognosticating, and surveillance of diseases, especially solid cancers. MiR-193a was shown to be directly pathogenic in an experimental mouse model of focal segmental glomerulosclerosis (FSGS) during the last decade. Its specific binding and downregulation of Wilm’s tumor-1 (WT-1), a transcription factor regulating podocyte phenotype, is documented. Also, miR-193a is a regulator switch causing the transdifferentiation of glomerular parietal epithelial cells to a podocyte phenotype in in vitro study. Interaction between miR-193a and apolipoprotein 1 (APOL1) mRNA in glomeruli (filtration units of kidneys) is potentially involved in the pathogenesis of common glomerular diseases. Since the last decade, there has been an increasing interest in the role of miR-193a in glomerular diseases, including diabetic nephropathy and membranous nephropathy, besides FSGS. Considering the lack of biomarkers to manage FSGS and diabetic nephropathy clinically, it is worthwhile to invest in evaluating miR-193a in the pathogenesis of these diseases. What causes the upregulation of miR-193a in FSGS and how the mechanism is different in different glomerular disorders still need to be elucidated. This narrative review highlights the pathogenic mechanisms of miR-193a elevation in various glomerular diseases and its potential use in clinical management. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Kidney Injury and Repair II)
Show Figures

Graphical abstract

Back to TopTop