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Special Issue "Inflammation and Oxidative Stress in Kidney Disease 2.0"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 January 2021).

Special Issue Editor

Dr. Peter Hamar
E-Mail Website
Guest Editor
Institute of Pathophysiology, Semmelweis University, Budapest, Hungary
Interests: triple negative breast cancer (TNBC); modulated-electrohyperthermia (mEHT); ischemia induced acute kidney injury (IRI-AKI); non-coding RNAs (miRNA, siRNA, lncRNA); the role of fibrinogen in cell stress
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Special Issue Information

Dear colleagues,

Ischemia-reperfusion injury (IRI) is the leading cause of acute kidney injury (AKI). IRI can lead to renal transplantation as well as circulatory and septic shock. Moreover, it contributes to contrast-induced nephropathy and can lead to chronic kidney disease in the long term. The initial injury is aggravated by subsequent inflammation due to the deliberation of danger-associated molecular patterns (DAMP) and their recognition via toll-like receptors (TLRs). TLRs activate the inflammasome, the interferon (IFN) response, and the subsequent cytokine release initiates inflammation associated with oxidative stress. Cell death is primarily necrotic during ischemia, but tissue damage due to necroptosis or apoptosis occurs during reperfusion. Bacterial endotoxin (lipopolysaccharide)-induced immune-paralysis can provide protection from an otherwise lethal ischemic injury; however, the molecular mechanisms of this cross-tolerance are largely unknown.

An increasing body of evidence suggests that these processes are regulated or modulated by non-coding RNAs (lncRNA, miRNA) and thus can be therapeutically influenced by RNA-based therapies (mRNA, siRNA, ASO). The role of miR-21 has been already well established in disease states, but influencing miR-21 expression did not provide the expected clinical benefit. New miRs and lncRNAs are emerging as potential therapeutic tools to reduce reperfusion injury and chronic kidney disease.

Dr. Peter Hamar
Guest Editor

Manuscript Submission Information

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Published Papers (1 paper)

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Review

Open AccessReview
MicroRNAs as Biomarkers and Therapeutic Targets in Inflammation- and Ischemia-Reperfusion-Related Acute Renal Injury
Int. J. Mol. Sci. 2020, 21(18), 6738; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186738 - 14 Sep 2020
Cited by 2 | Viewed by 689
Abstract
Acute kidney injury (AKI), caused mainly by ischemia-reperfusion, sepsis, or nephrotoxins (such as contrast medium), is identified by an abrupt decline in kidney function and is associated with high morbidity and mortality. Despite decades of efforts, the pathogenesis of AKI remains poorly understood, [...] Read more.
Acute kidney injury (AKI), caused mainly by ischemia-reperfusion, sepsis, or nephrotoxins (such as contrast medium), is identified by an abrupt decline in kidney function and is associated with high morbidity and mortality. Despite decades of efforts, the pathogenesis of AKI remains poorly understood, and effective therapies are lacking. MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression at the posttranscriptional level to control cell differentiation, development, and homeostasis. Additionally, extracellular miRNAs might mediate cell–cell communication during various physiological and pathological processes. Recently, mounting evidence indicates that miRNAs play a role in the pathogenesis of AKI. Moreover, emerging research suggests that because of their remarkable stability in body fluids, microRNAs can potentially serve as novel diagnostic biomarkers of AKI. Of note, our previous finding that miR-494 is rapidly elevated in urine but not in serum provides insight into the ultimate role of urine miRNAs in AKI. Additionally, exosomal miRNAs derived from stem cells, known as the stem cell secretome, might be a potential innovative therapeutic strategy for AKI. This review aims to provide new data obtained in this field of research. It is hoped that new studies on this topic will not only generate new insights into the pathophysiology of urine miRNAs in AKI but also might lead to the precise management of this fatal disease. Full article
(This article belongs to the Special Issue Inflammation and Oxidative Stress in Kidney Disease 2.0)
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