Mechanisms of kidney fibrosis and the role of antifibrotic therapies

Purpose of review Kidney fibrosis is a common observation in human and experimental models of kidney disease and contributes to the progressive loss of kidney function. This review discusses the recent recognition of the role of podocytes in the development of common glomerular disease and focuses on the basis for new antifibrotic therapies. Recent findings A growing body of evidence indicates that changes in the structure and function of podocytes are involved in the development and progression of kidney disease. The changes include podocyte de-differentiation, podocyte-mediated endothelial dysfunction and podocyte-incluced epithelial-mesenchymal transition, all contributing to the development of kidney fibrosis. Furthermore, new antifibrotic strategies aiming at the transforming growth factor-beta, connective tissue growth factor, angiotensin (1 7), and advanced glycation endproducts/receptors; advanced glycation endproducts signaling pathways are being developed. Summary Podocytes are recognized to play a key role in the development of kidney fibrosis. New antifibrotic therapies are rapidly progressing toward definitive clinical trials but will need to be tested on top of the existing therapy of renin-angiotensin system inhibition. Novel approaches targeting podocyte function would be a promising approach for early stages of the disease.