Given that PPIB is critical for collagen folding and its knockdown results in loss of collagen (33, 34), we next evaluated the effect of SfA in fibrosis, which is characterized by excessive production of collagen type I. PPIB catalyzes the rate-limiting step of procollagen triple helix folding within the collagen prolyl 3-hydroxylation complex, which is comprised of prolyl 3-hydroxylase 1 (P3H1), cartilage-associated protein (CRTAP), and PPIB (33–35). This evidence concerns the gene P3H1 and fibrosis.