# MicroRNA Regulation in Kidney Interstitial Fibrosis

## TL;DR

This review explores how microRNAs regulate kidney fibrosis and their potential as biomarkers and therapies for chronic kidney disease.

## Contribution

The paper integrates miRNA functions in fibrotic pathways and disease-specific roles in chronic kidney disease.

## Key findings

- miRNAs regulate fibrotic pathways through multiple cell types in kidney disease.
- Disease-specific miRNA dysregulation is observed in diabetic kidney disease and other CKD types.
- miRNAs show promise as biomarkers and therapeutic targets for CKD.

## Abstract

MicroRNAs (miRNAs) are small non-coding RNAs that play central roles in post-transcriptional gene regulation and cellular homeostasis maintenance. Dysregulation of miRNA expression is increasingly recognized as a key contributor to tissue injury during the acute phase and to disease progression in the chronic phase. Chronic kidney disease (CKD) commonly progresses and ultimately leads to kidney failure through interstitial fibrosis, which is the final common pathway of CKD progression. Interstitial fibrosis is driven not only by fibroblast activation but also by phenotypic transitions in injured tubular epithelial cells, infiltrating macrophages, and peritubular capillary cells. These multifaceted cellular pathways induce and exacerbate interstitial fibrosis, and several miRNAs have been identified as important regulators of these pathways. In addition to fibrotic pathophysiological features, disease-specific dysregulation of miRNAs has been increasingly detected in various causes of CKD, including diabetic kidney disease, chronic glomerulonephritis, and nephrosclerosis. In this review, we provide an integrated overview of miRNA-mediated regulation in CKD, with particular emphasis on cell lineage functions within fibrotic pathways and disease-specific roles. Finally, we discuss the emerging potential of miRNAs as biomarkers and therapeutic targets for CKD and highlight future research directions.