Organ fibrosis involves a complex interplay between diverse cell types and signaling pathways that ultimately leads to the pathologic accumulation of excessive extracellular matrix, subsequently resulting in organ dysfunction. In recent years, the first drugs for the treatment of idiopathic pulmonary fibrosis have been approved; however, there is a major unmet need for effective antifibrotic therapies across organs. Despite the complexity of the fibrotic process in different tissues, certain features are shared and may form the basis for future therapeutic strategies. This Review will highlight these shared characteristics, cell states, and signaling pathways across organs with the goal of highlighting potential antifibrotic strategies.
