Fibrosis is an irreversible process that occurs in all major organs in the body; however, excessive fibrosis results in organ dysfunction and possible death. This process involves robust proliferation of fibroblasts and, in turn, excessive accumulation of extracellular matrix (ECM) within and around damaged tissues, leading to abnormal architectural remodeling (Cannito S, Novo E, Parola M, Adv Drug Deliv Rev 121:57–84, 2017; Kendall RT, Feghali-Bostwick CA, Front Pharmacol 5:123, 2014). The fibrotic process can be triggered and initiated by various fibrotic factors such as transforming growth factor-β (TGF-β) (Travis MA, Sheppard D, Annu Rev Immunol 32:51–82, 2014), members of the connective tissue growth factor (CTGF) family as well as the platelet-derived growth factor (PDGF) family (Wynn TA, J Pathol 214(2):199–210, 2008). Despite advanced modern medicine, there has been no satisfactory progress in inhibiting or reversing the progression of fibrosis. Therefore, research continues to uncover advanced antifibrotic therapeutics. Among the many known factors involved in the development and progression of organ fibrosis, circular RNAs (circRNAs) have recently drawn attention as having an essential role in organ fibrosis. Their critical involvement in fibrosis opens a new avenue of promising drug therapy. This chapter summarizes the current research progress on the biological function and underlying molecular mechanism(s) of circRNAs in regulating organ fibrosis, including heart, lung, and kidney. Furthermore, we discuss the contribution of circRNAs to antifibrotic therapy and what its future holds.