Circular RNAs in Acute Kidney Injury: Roles in Pathophysiology and Implications for Clinical Management

Acute kidney injury (AKI) is a common clinical condition, results in patient morbidity and mortality, and incurs considerable health care costs. Sepsis, ischaemia-reperfusion injury (IRI) and drug nephrotoxicity are the leading causes. Mounting evidence suggests that perturbations in circular RNAs (...

Full description

Saved in:
Bibliographic Details
Published in:International journal of molecular sciences Vol. 23; no. 15; p. 8509
Main Authors: So, Benjamin Y. F., Yap, Desmond Y. H., Chan, Tak Mao
Format: Journal Article
Language:English
Published: Basel MDPI AG 31-07-2022
MDPI
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Acute kidney injury (AKI) is a common clinical condition, results in patient morbidity and mortality, and incurs considerable health care costs. Sepsis, ischaemia-reperfusion injury (IRI) and drug nephrotoxicity are the leading causes. Mounting evidence suggests that perturbations in circular RNAs (circRNAs) are observed in AKI of various aetiologies, and have pathogenic significance. Aberrant circRNA expressions can cause altered intracellular signalling, exaggerated oxidative stress, increased cellular apoptosis, excess inflammation, and tissue injury in AKI due to sepsis or IRI. While circRNAs are dysregulated in drug-induced AKI, their roles in pathogenesis are less well-characterised. CircRNAs also show potential for clinical application in diagnosis, prognostication, monitoring, and treatment. Prospective observational studies are needed to investigate the role of circRNAs in the clinical management of AKI, with special focus on the safety of therapeutic interventions targeting circRNAs and the avoidance of untoward off-target effects.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms23158509