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 2694
Special Issue Editor
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
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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
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