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. 2019 Sep 23;8(10):1130. doi: 10.3390/cells8101130

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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TGFβ and BMP interplay in kidney, lungs, liver and heart fibrosis. (a) In tubular epithelial cells TGFβ and BMP7 reciprocally oppose each other’s effects on fibrosis through regulating the expression of key miRNAs with antagonist functions. In mesangial cells BMP7 counteracts TGFβ pro-fibrotic activity via a SMAD5/6 mechanism that prevents SMAD3 nuclear accumulation, and subsequent MMP2 inhibition. (b) BMP2 can prevent the TGFβ-induced trans-differentiation of HSCs in MFBs through downregulating the expression of TGFβ itself and its receptors. By a more indirect mechanism (as in heart fibrosis), BMP2 can also counteract TGFβ-induced EMT. Arrows are colored according to organs of reference. HSC = hepatic stellate cell; FB = fibroblast; MFB = myofibroblast; EC = epithelial cell. Fibrosis limiting/promoting ligands are enclosed in green/orange boxes, respectively.