The Intersection of Acute Kidney Injury and Non-Coding RNAs: Inflammation

Abstract

Acute renal injury (AKI) is a complex clinical syndrome, involving a series of pathophysiological processes, in which inflammation plays a key role. Identification and verification of gene signatures associated with inflammatory onset and progression are imperative for understanding the molecular mechanisms involved in AKI pathogenesis. Non-coding RNAs (ncRNAs), involved in epigenetic modifications of inflammatory responses, are associated with the aberrant expression of inflammation-related genes in AKI. However, its regulatory role in gene expression involves precise transcriptional regulation mechanisms which have not been fully elucidated in the complex and volatile inflammatory response of AKI. In this study, we systematically review current research on the intrinsic molecular mechanisms of ncRNAs that regulate the inflammatory response in AKI. We aim to provide potential research directions and strategies for developing ncRNA-targeted gene therapies as an intervention for the inflammatory damage in AKI.

Prostaglandin Transporter and Dipeptidyl Peptidase-4 as New Pharmacological Targets in the Prevention of Acute Kidney Injury in Diabetes: An In Vitro Study

“…In addition, PTC expression of adhesion molecules is also required for the firm attachment of leukocytes previously directed to them through chemotaxis [ 4 ]. The acquisition by PTCs of these pro-inflammatory properties leads to the recruitment of immune cells, thereby aggravating the damage of PTCs through leukocyte-dependent inflammatory responses [ 43 ]. In this context, given its well-established role as an inflammatory mediator, PGE 2 is highly likely to be involved in the instauration and progression of AKI, as shown by the known activation of the renal inflammatory COX-2/PGE 2 cascade in experimental models of AKI [ 9 ] and our own results.…”

Steroidogenic factor 1 promotes cuproptosis in renal tubular epithelial cells during acute kidney injury

“…The common causes of AKI include hypovolemia, infection and drugs [2], and Coronavirus disease 2019 pneumonia is also one of the important causes of the condition. The main mechanisms of kidney damage in AKI include oxidative stress [3], in ammatory reaction [4], endothelial damage, microvascular dysfunction [5], mitochondrial damage [6], and ultimately death of renal tubular epithelial cells (RTECs).…”