MicroRNAs in acute kidney injury.

Pei-Chun Fan,Yung-Chang Chen,Pao-Hsien Chu,Chia-Chun Chen,Yu-Sun Chang

doi:10.1186/s40246-016-0085-z

Pei-Chun Fan, Yung-Chang Chen + Show 3 more

Open Access

https://doi.org/10.1186/s40246-016-0085-z

Copy DOI

Abstract

Acute kidney injury (AKI) is an important clinical issue that is associated with significant morbidity and mortality. Despite research advances over the past decades, the complex pathophysiology of AKI is not fully understood. The regulatory mechanisms underlying post-AKI repair and fibrosis have not been clarified either. Furthermore, there is no definitively effective treatment for AKI. MicroRNAs (miRNAs) are endogenous single-stranded noncoding RNAs of 19~23 nucleotides that have been shown to be crucial to the post-transcriptional regulation of various cellular biological functions, including proliferation, differentiation, metabolism, and apoptosis. In addition to being fundamental to normal development and physiology, miRNAs also play important roles in various human diseases. In AKI, some miRNAs appear to act pathogenically by promoting inflammation, apoptosis, and fibrosis, while others may act protectively by exerting anti-inflammatory, anti-apoptotic, anti-fibrotic, and pro-angiogenic effects. Thus, miRNAs have not only emerged as novel biomarkers for AKI; they also hold promise to be potential therapeutic targets.

Highlights

Acute kidney injury Acute kidney injury (AKI) is a complex syndrome that occurs in a variety of settings with clinical manifestations ranging from a minimal elevation in serum creatinine to anuric renal failure
The evidence accumulated over the past two decades shows that miRNAs play a critical role in the post-transcriptional regulation of almost all biological cell functions, including proliferation, differentiation, metabolism, and apoptosis [4]. miRNAs, which are expressed in a tissue-specific manner, are fundamental to normal development and physiology [4] and are involved in the pathologic pathways of many disease models
Some of them contribute to the pathogenesis by regulating apoptosis and inflammation, to amplifying or reduce acute injury responses, while others regulate fibrosis and angiogenesis, to participate in renal recovery or the progression to fibrosis

Summary

Introduction

Acute kidney injury Acute kidney injury (AKI) is a complex syndrome that occurs in a variety of settings with clinical manifestations ranging from a minimal elevation in serum creatinine to anuric renal failure. In rodent models of renal IRI and streptozocin (STZ)-induced diabetic nephropathy, the levels of miR-10a are increased decreased in urine and kidney tissue, respectively [15, 16]. The members of the miR-17 family have been shown to be induced by pro-inflammatory cytokines, and their tissue expressions are increased in rodent models of renal IRI [19, 20]. IRI, folic acid, CdCl2, arsenic trioxide, AA, K2Cr2O7, cisplatin, UUO, allograft rejectiona, renal fibrosisa miR-142-3p T, in vitro

Results

Conclusion