Overexpression of Smad7 Results in Severe Pathological Alterations in Multiple Epithelial Tissues

The study from 21 years ago found that overexpression of Smad7 in mice led to severe pathological alterations in multiple epithelial tissues, including significant delays and abnormalities in hair follicle formation. The Smad7 transgene was highly expressed in the epidermis and hair follicles, causing a significant reduction in the protein levels of TGFBR, ActR, and BMPR in these areas. This overexpression also resulted in severe thymic atrophy and eye development defects. The study concluded that Smad7 overexpression directly reduces certain receptor proteins of TGFB, activin, and BMP, acting as a potent in vivo inhibitor of signal transduction by the TGFB superfamily in certain epithelial tissues.