TGFB1 and chronic kidney disease: Protein inactivation and dysfunction linked to the dicarbonyl proteome may accelerate CKD development [10] Higher production of MG consumes more GSH, and eventually, a depleted status of GSH may occur, resulting in an imbalance of the in vivo oxido-reduction status [31] ROS may upregulate profibrotic molecules such as transforming growth factor-beta 1 and plasminogen activator inhibitor-1 [17].