Carol Artlett

My research is primarily focused on fibrosis and the signaling pathways that not only drive the expression of collagen but promote procollagen export from the endoplasmic reticulum. This interest includes several areas of expertise involving inflammasome signaling, and the role of miR-155 and IL-1 in promoting fibrosis. More recent work has focused on the endoplasmic reticulum and the role of TANGO1 in procollagen export. TANGO1 accompanied by cTAGE5 is needed for the expansion of tubules for protein export to the Golgi apparatus. Without these two proteins, collagen and indeed a milieu of other high molecular weight extracellular proteins cannot be exported and then secreted from the cell. Our research is focused on pathways that intersect with the inflammasome that induce TANGO1 and cTAGE5 expression and thereby promote fibrosis. Understanding these mechanisms is crucial to developing effective therapeutics that will control this pathology. During our research, we have identified a small molecule that is anti-fibrotic because it targets TANGO1 expression. We believe this could be an effective therapeutic for the fibrotic autoimmune disease systemic sclerosis (scleroderma). In these patients where there is uncontrolled systemic fibrosis that severely affects their quality of life leading to an early death post-diagnosis.