Abstract
Diseases affecting the glomerulus, the filtration unit of the kidney, are a major cause of chronic kidney disease. Glomerular disease is characterised by injury of glomerular cells and is often accompanied by an inflammatory response that drives disease progression. New strategies are needed to slow the progression to end-stage kidney disease, which requires dialysis or transplantation. Thymosin β4 (Tβ4), an endogenous peptide that sequesters G-actin, has shown potent anti-inflammatory function in experimental models of heart, kidney, liver, lung, and eye injury. In this review, we discuss the role of endogenous and exogenous Tβ4 in glomerular disease progression and the current understanding of the underlying mechanisms.