Troglitazone Suppresses Collagen Synthesis via Expression of the Downstream

important endogenous anti-fibrotic defense mechanism. Troglitazone, a PPAR-γ agonist, has been used to suppress the formation of keloids and growth of hypertrophic scar fibroblasts. Indeed, the PPAR-γ agonist was able to inhibit collagen I expression in hypertrophic scar fibroblasts, which clearly demonstrates its therapeutic potential, and clarification of the underlying molecular mechanisms could further indicate the usefulness of the PPAR-γ agonists in the treatment of keloids. Moreover, increasing evidence has suggested that aberrant expression of miRNAs leads to the development and progression of fibrosis diseases. Thus, fully understanding the biological functions and molecular mechanisms of miRNAs in the regulation of fibrosis could provide insight for advancements in the diagnosis and treatment of fibrosis. This commentary briefly summarizes the current evidence for the ability of PPAR-γ agonist troglitazone to suppress collagen synthesis and regulate miRNA expression and downstream targets in cells.