Although our main focus was the modification of ROS levels as a mediator of downstream high-glucose-induced TGF-β1 signaling [20], we discovered that momordicine I alleviated the production of hyperglycemia-induced ROS and might block the activation of high-glucose-induced cardiac fibroblast by inhibiting ROS and its downstream TGF-β1 signal. This evidence concerns the gene TGFB1 and Hyperglycemia.