High doses of TGF-β potently suppress type I collagen via the transcription factor CUX1

摘要

Uncontrolled expression of collagen often leads to tissue scarring and loss of organ function. In this study, we identify a molecular mechanism that may enable us to switch off collagen production when unnecessary (i.e., fibrosis). We conclude that CUX1, which is a CCAAT binding factor displacement protein, may serve as a therapeutic target in treating fibrosis.