MicroRNAs (
miRNAs) are endogenous short non-coding RNAs that regulate most of important cellular processes by inhibiting gene expression through the post-transcriptional repression of their target mRNAs. In kidneys,
miRNAs have been associated in renal development, homeostasis, and physiological functions. Results from clinical and experimental animal studies demonstrate that
miRNAs play essential roles in the pathogenesis of various renal diseases.
Chronic kidney diseases (CKD) is characterized by renal
fibrosis.
Transforming growth factor beta (TGF-β) is recognized as a major mediator of renal
fibrosis because it is able to stimulate the accumulation of extracellular matrix (ECM)
proteins to impair normal kidney function. Recently, emerging evidence demonstrate the relationship between TGF-β signaling and
miRNAs expression during renal diseases. TGF-β regulates expression of several
microRNAs, such as miR-21, miR-192, miR-200, miR-433, and miR-29. MiR-21, miR-192, and miR-433 which are positively induced by TGF-β signaling play a pathological role in
kidney diseases. In contrast, members in both miR-29 and miR-200 families which are inhibited by TGF-β signaling protect kidneys from renal
fibrosis by suppressing the deposition of ECM and preventing epithelial-to-mesenchymal transition, respectively. Clinically, the presence of
miRNAs in blood and urine has been examined to be early
biomarkers for detecting renal diseases. From experimental animal studies of CKD, targeting
microRNAs also provides evidence about therapeutic potential of
miRNAs during renal diseases. Now, it comes to the stage to examine the exact mechanisms of
miRNAs during the initiation and progression of renal diseases. Therefore, determining the function of
miRNAs in renal
fibrosis may facilitate the development of both early diagnosis and treatment of renal diseases.