Fibrosis refers to a process involving the accumulation of extracellular matrix components. It could happen in chronic organ injury or during the recovery of acute organ injury. The severity of fibrosis interferes with the function of the organ involved. Numerous studies have been carried out to explore the mechanism of fibrosis, including parenchyma injury, fibrillar ECM accumulation, fibroblast activation, microvasculature rarefaction, and a mononuclear infiltrate. Unfortunately, its underlying mechanism is at largely unknown. The studying of noncoding RNAs has provided novel insight for circRNA-miRNA-mRNA in learning disease progress. Emerging evidence has shown that circRNA is related to fibrosis activity and could potentially be a monitoring factor for fibrosis or, more excitingly, could be a target for treatment. In this chapter, we will first present the basic mechanism of organ fibrosis. Then we will focus on the recent studies about how circRNA dysregulation contributes to organ fibrosis. Finally, the advantages and potential challenges of circRNA-based therapeutics for the treatment of fibroproliferative diseases will be discussed.
Keywords: Fibrosis; circRNA.