The role of activins in TGFβ profibrotic signaling in chronic kidney disease
Chronic kidney disease (CKD) is a global health condition affecting upwards of 14% of individuals worldwide. Characterized by stages of decreased kidney function and increased albuminuria, dialysis and kidney transplantation are the only existing therapies. Current research has established the role of TGFβ profibrotic signaling in a dysregulated wound healing response, resulting in the excessive accumulation of extracellular matrix components in kidney glomeruli and interstitium. This accumulation detrimentally and often irreversibly affects kidney function. While efforts have been made to investigate the efficacy and feasibility of blocking TGFβ1 as a therapeutic target, the consequences of inhibition result in many adverse side effects. Recent studies have identified a potential role for activins in profibrotic signaling. As cytokines in the TGFβ superfamily, activins play an important role in cell growth and differentiation and are shown to fine-tune fibrotic pathways. Here, we review the mechanisms of action involving activins and renal disease.