Chronic organ injuries are accompanied by a dysregulated scarring process called "Fibrosis" that is characterized by hyperactivity of TGF-beta resulting in an imbalance of extracellular matrix homeostasis and accumulation of fibrosis-associated proteins. These changes are due to a specialized matrix-expressing cell type, i.e. the myofibroblast, which is derived from independent cellular sources. Beside resident quiescent fibroblasts that become activated, circulating bone-marrow-derived fibrocytes are attracted by the injured organ. Additionally, epithelial cells transit into mesenchymal cells in a process termed epithelial-to-mesenchymal transition. Furthermore, mesothelial cells leave their peripheral location and acquire a fibrogenic phenotype via mesothelial-to-mesenchymal transition. Numerous independent studies have consistently demonstrated that BMP-7 interferes with TGF-betasignaling and a diverse set of matricellular proteins (e.g. CCN proteins), Endoglin, Betaglycan, BAMBI and the members of the repulsive guidance molecule family that modulate cellular proliferation, migration, adhesion and extracellular matrix production. This protein network might therefore depict novel targets for treatment of fibrotic lesions. We here summarize recent knowledge of BMP-7 function and discuss attempts to use this cytokine as a drug to reverse TGF-beta-induced fibrogenesis.