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. Author manuscript; available in PMC: 2015 Sep 2.
Published in final edited form as: Connect Tissue Res. 2012 Aug 23;54(1):5–13. doi: 10.3109/03008207.2012.715700

Figure 5.

Figure 5

Proposed model of mechanisms involving TGFβ1 and BMP4 signaling to explain the physiological changes in Bgn null mice. In brief, BGN deficiency causes elevated TGFβ1 levels but decreased BMP4 sensitivity in this hyperlipidemic mouse model. Both TGFβ1 and BMP4 are pro-fibrotic. The lack of pathological changes such as liver fibrosis or glomerulosclerosis in Bgn null mice could be due to opposing actions from increased TGFβ1 versus decreased BMP4 signaling. Instead, reduced BMP4 activity may improve albuminuria. However, TGFβ1 and BMP4 exert opposite functions in adipogenesis, so both TGFβ1 elevation and BMP4 deactivation play negative roles in adipogenesis, potentially contributing to the striking reduction in adiposity.